Philip Lerche Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH, 43210, USA Animals presenting for ophthalmic surgery pose several challenges to the anesthetist, including the effects of anesthetic drugs on intraocular pressure (IOP) and tear production, patient positioning, reflexes that may occur during intraoperative manipulation of the eye, the effect of topically or systemically administered ophthalmic drugs, and, in many older animals, coexisting disease. Additionally, procedures that require the globe to be positioned centrally within the orbit for optimal surgical access (e.g., cataract removal and extensive conjunctival surgery) frequently require the use of neuromuscular blocking agents (NMBAs) and mechanical ventilation. IOP is a function of the relationship between aqueous humor production and its drainage, the majority of which occurs in cats and dogs via the trabecular meshwork of the anterior chamber angle [1]. This relationship can be quantified as follows: Ocular perfusion pressure determines the blood supply to the retina and optic nerve and is defined as the difference between mean arterial blood pressure and IOP. Thus, an increase in IOP can lead to a decrease in optic nerve function, leading to a potential loss of vision if not recognized and treated. A major goal when anesthetizing animals that present with preexisting glaucoma for both ophthalmic and nonophthalmic surgeries is to prevent unwanted increases in IOP. It is also imperative to prevent sudden increases in IOP in patients that present with partial or imminent loss of globe integrity (e.g., descemetocele, trauma, deep corneal ulcer) to prevent complete rupture. The physical, physiologic, and pharmacologic causes of increased IOP are presented in Table 12.1. There are several factors that may increase IOP via increased central venous pressure (CVP). Physical restraint of a struggling patient as well as inadvertent pressure on the jugular veins may cause increased CVP and IOP. Vomiting, straining, and coughing all increase IOP by temporarily increasing CVP [2]. Coughing or gagging during stimulation of the larynx and pharynx during endotracheal intubation transiently increases IOP [3]. Thus, in patients with increased IOP, intubation during very light planes of anesthesia should be avoided. The use of topical lidocaine applied to the glottis or the administration of intravenous lidocaine (2 mg kg−1 IV) to decrease stimulation during intubation is also prudent [4]. The presence of preexisting glaucoma and the development of hypercarbia and/or hypoxemia all lead to increases in IOP [5]. As with all anesthetic patients, it is important to carefully monitor ventilatory status as well as oxygenation and supplement oxygen and offer ventilatory support as needed. However, oxygen supplementation should be delivered with caution, as any pressure applied to the eyes via the eyelids such as digital compression or placement of a face mask causes a direct increase in IOP. Elevating the head above the rest of the body will tend to decrease IOP, while, conversely, lowering the head below the body (i.e., Trendelenburg position) may elevate IOP. In the postanesthetic period, measures to avoid acute increases in IOP must continue to be considered. It is important to note that increases in IOP have been shown to occur in approximately 20% of dogs following cataract surgery [6]. It is therefore prudent to maintain intravenous access for administration of diuretics or for sedation if anterior chamber paracentesis is needed to relieve high IOP after anesthetic recovery. Table 12.1 Factors causing an increase in IOP. a If myoclonus occurs b High dosage or as sole agent Many anesthetic drugs directly decrease or do not change IOP; however, side effects such as vomiting (opioids, alpha‐2‐adrenergic receptor agonists), hypercapnia (propofol, alfaxalone, opioids, alpha‐2‐adrenergic receptor agonists, inhalants), or myoclonus (etomidate) may cause IOP to increase. Ketamine and succinylcholine have also been shown to increase IOP [7]. Both propofol and alfaxalone when given as a single IV bolus caused an initial small, transient increase in IOP 2 min after administration to dogs followed by a significant decrease in IOP for 25 min [8]. In another study, alfaxalone administration increased IOP in healthy dogs, and the highest IOP recorded was associated with intubation [9]. In dogs, atropine given subcutaneously and topically is correlated with a decrease in tear production [10, 11]. Similarly, general anesthesia has been found to decrease tear production for up to 24 h after general anesthesia; anesthetic events lasting more than 2 h had a significantly greater impact on postoperative tear production than shorter procedures [12]. Conversely, a different study demonstrated that tear production returned to normal immediately after short (1 h) and long (4 h) anesthetic episodes when either isoflurane or desflurane was used as the sole anesthetic agent [13]. Conflicting results of these studies may be due to a difference in methods, as multiple drugs (premedication, injectable induction agents) were used in the former study, including atropine, which may account for the different findings. Alfaxalone and propofol have been shown to reduce tear production [8]. General anesthesia with sevoflurane after administration of morphine, acepromazine, or after no premedication also reduced tear production [14]. Tear production was decreased in cats after acepromazine and xylazine sedation [15]. Yet another study reported that, in the intensive care unit setting, tear production was reduced by approximately 50% in dogs with no history of eye disease and no recent anesthetic episodes [16]. This should be taken into consideration when hospitalizing dogs prior to surgery for disease management (e.g., diabetes mellitus or chronic renal disease). In cases of unilateral ocular surgery, the unaffected eye should be protected and treated with a topical artificial tear ointment or gel. In cats, application of an eye gel caused less postoperative irritation, as identified by reduced blepharospasm, compared to an ointment [17]. Tear production was decreased after surgery regardless of treatment type. Tear production was decreased in cats anesthetized with a medetomidine–ketamine combination, and within 15 min of atipamezole administration returned to normal [18]. The head of the patient is typically somewhat distant to the anesthetist during ophthalmic surgery, resulting in several challenges (Figure 12.1). First, it is not possible to assess anesthetic depth using the palpebral reflex, globe position within the orbit, or jaw tone. The anesthetist must rely on cardiovascular and respiratory monitoring and feedback from the surgeon about response to surgery as indicators of anesthetic depth change. Second, the endotracheal tube, endotracheal tube connector, and patient end of the breathing system are not visible or easily accessed. This makes it more difficult to detect accidental extubation (especially if capnometry is not utilized), the presence of leaks, and disconnections. Third, it may not be possible to place or access monitoring equipment on the tongue (pulse oximeter), in the esophagus (temperature probe, stethoscope), or connected to the breathing system (capnometry) depending on the distance from the anesthetic monitor to the patient’s head. Finally, movement of the surgery table or patient by the anesthetist during surgery may make it challenging for the ophthalmologist, particularly when an operating microscope is being used, as small movements will be greatly magnified in the surgeon’s field of vision. Pressure or traction on the globe or nearby extraocular tissues during surgery may induce an oculocardiac reflex (OCR) via the trigeminal (cranial nerve V, afferent limb) and vagal (cranial nerve X, efferent limb) nerves that results in the development of dysrhythmias. The most common dysrhythmia noted is bradycardia; however, ventricular ectopy and asystole may also occur. The presence of hypercarbia increases the likelihood of OCR occurring [19]. Initial management involves communicating the occurrence of OCR to the surgeon, who should stop manipulating the eye immediately. If the OCR persists or is severe, treatment with an anticholinergic may be necessary. Commencement of cardiopulmonary resuscitation should immediately be initiated in the case of asystole. In a retrospective study of 145 dogs undergoing enucleation, OCR occurred in approximately 5% of cases [20]. Age, breed, and preoperative anticholinergic treatment were not associated with an increase in the prevalence of OCR, whereas retrobulbar nerve block decreased the chance of OCR occurring. Figure 12.1 Typical setup of an ophthalmology operating room, with the animal’s head placed distant from the anesthesia machine and the anesthetist. Many patients that present for ophthalmic surgery have received ophthalmic drugs prior to surgery. Thus, it is important to understand their potential physiologic impact. Systemically administered drugs are much more likely to result in side effects; however, systemic absorption of topically applied drugs can occur. It is important to recognize the potential for side effects of ophthalmic drugs administered by any route, so that when they occur, they can be managed appropriately. Cholinergic agents (e.g., pilocarpine) increase the rate of aqueous humor outflow. If absorbed systemically, unwanted parasympathetic effects such as bradydysrhythmias and bronchoconstriction may be seen [1]. Topically applied adrenergic agonist drugs (e.g., epinephrine and phenylephrine) may lead to systemic hypertension and tachycardia [21]. Adrenergic antagonists (e.g., timolol) will have the opposite effect if absorbed (i.e., bradycardia). Inhibition of carbonic anhydrase (CA) by systemic administration of acetazolamide leads to a decrease in aqueous humor formation [22]. The CA enzyme is also present in the kidney, and its inhibition interferes with renal electrolyte exchange mechanisms resulting in a decrease in bicarbonate reabsorption. This leads to hyperchloremia, hypokalemia, and metabolic acidosis. Topical CA inhibitors such as brinzolamide have generally superseded the systemic use of acetazolamide, as they have minimal side effects. Diuretic use (e.g., mannitol) may lead to an initial volume expansion, which, in patients with moderate to severe cardiovascular disease, may cause pulmonary overload and edema, or congestive heart failure [23]. Ultimately dehydration, hyponatremia, and metabolic acidosis may occur. Prolonged corticosteroid drop use may depress the adrenal cortex and possibly result in hypoadrenocorticism, thus decreasing an animal’s ability to respond appropriately to the stress of anesthesia and surgery [24]. Hypoadrenocorticism usually results in hyponatremia, hyperkalemia, and dehydration, as well as lethargy and inappetence (see Chapter 9). A patient presenting for nonurgent ophthalmic surgery with clinical symptoms and blood work that are suspicious of hypoadrenocorticism should undergo further diagnostics and treatment. In the case of a patient where hypoadrenocorticism is suspected that needs urgent or emergency ophthalmic procedures, every effort should be made to correct hydration and electrolyte status prior to anesthesia. It may be necessary to administer supplemental corticosteroids prior to anesthesia (e.g., prednisolone 1–2 mg kg−1 IV). Topical atropine drops may result in tachydysrhythmias and bronchodilation if absorbed into the systemic circulation [25]. If abnormal cardiac rhythms are detected during the preanesthetic physical examination, an electrocardiogram should be performed to document and identify the arrhythmias. If possible, surgery can be postponed so that treatment of a dysrhythmia can be initiated prior to anesthesia (see Chapter 1). The electrocardiogram should be closely monitored during surgery in the case of atropine being applied topically. Patients presenting for ophthalmic surgery range in age, and older animals often have coexisting diseases of other body systems. Renal, cardiovascular, and endocrine diseases are more common in older patients and should be managed appropriately (see corresponding chapters in this book). For example, the incidence of cataract formation in diabetic dogs is high, and these patients often present for anesthesia to remove sclerotic lenses and replace them with prosthetics. It is important to monitor blood glucose frequently in these patients because withholding food and the unavoidable stress associated with the perioperative period (being in the unfamiliar environment of the veterinary clinic) may lead to unexpected hyperglycemia or hypoglycemia, and both may occur within the same anesthetic episode. The anesthetist should be prepared to treat hypoglycemia by adding dextrose to IV fluids (2.5–5% solutions, as needed, are usually adequate). Severe hyperglycemia (blood glucose >450 mg dl−1) can be treated with regular insulin intraoperatively [26]
12
Anesthesia for Ophthalmic Patients
Introduction
Intraocular Pressure
Physical
Physiologic
Pharmacologic
Pressure on eyelids (e.g., face mask)
Vomiting
Coughing
Succinylcholine
Etomidatea
Endotracheal intubation
Preexisting glaucoma
Ketamineb
Excessive restraint and struggling
Hypoxemia
Hypercapnia
Nitrous oxide
Pressure on the jugular veins
Head below body
Cataract surgery
Tear Production
Patient Positioning
Oculocardiac Reflex (Aschner Reflex)
Ophthalmic Drugs
Drugs Used to Treat Glaucoma
Topical Corticosteroids
Drugs Used to Dilate the Pupil
The Presence of Coexisting Disease
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