ANESTHESIA AND INTRAOCULAR PRESSURE * DERYCK ... - NCBI

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ever, diplopia may persist up to 30 minutes during the recovery phase, causing anxiety ... a slight transient fall in intraocular pressure in normal eyes.This effect.
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ANESTHESIA AND INTRAOCULAR PRESSURE * DERYCK DUNCALF, M.B., F.F.A.R.C.S. Director, Anesthesiology Residency Training Program Montifiore Hospital and Medical Center Professor of Anesthesiology Albert Einstein College of Medicine Bronx, N. Y.

FOR intraocular procedures such as the extraction of cataracts it is desirable to achieve a normal or reduced intraocular pressure before the eye is opened. If the pressure is high at the time of the incision, the ocular contents: namely, the iris, lens, vitreous, and retina, may be expelled through the wound because of the sudden loss of pressure. Sudden release of intraocular tension also increases the likelihood of rupture of a sclerotic short posterior ciliary artery in the choroid; this may create an expulsive hemorrhage, causing loss of ocular contents. Once the eye has been opened, external pressure on the eye or vascular congestion of the uveal tract will tend to cause prolapse of ocular contents through the wound. It is apparent, then, that continuous control of intraocular pressure is a most important requirement of intraocular procedures. Techniques of anesthesia which have a tendency to lower intraocular pressure directly, or at least prevent its elevation, will often minimize vascular congestion of the eye and of the other orbital contents. Consequently, an anesthetic which is appropriate for intraocular surgery should also be suitable for ophthalmic operations in the course of which the coats of the eye are not divided. Moreover, should the sclera be inadvertently incised, for example during an operation for strabismus, it would be desirable to have the intraocular pressure within the normal range. Anesthetics, including muscle relaxants, may have both direct and indirect effects on intraocular pressure. For example, d-tubocurarine chloride lowers intraocular pressure directly by relaxing the extraocular *Presented at a combined meeting on Anesthesia in Ophthalmology held by the Section of Anesthesiology and Resuscitation of the New York Academy of Medicine and the New York Clinical Society of Ophthalmologists at the Academy March 4, 1974.

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muscles." 2 However, if the concomitant paralysis of the respiratory muscles is permitted to cause hypoventilation, which leads to hypercarbia and hypoxemia, these secondary changes may themselves elevate intraocular pressure. In addition to the indirect effects of anesthetics on intraocular pressure mediated through respiratory mechanisms, the consequences of possible hemodynamic changes resulting from anesthesia should also be considered. Changes in both arterial and central venous blood pressures are not uncommon during anesthesia. Changes in arterial pressure are relatively unimportant, since any increase in arterial pressure results in the displacement of aqueous humor from the anterior chamber and blood from the choroid. In contrast, any increase in venous pressure is transmitted directly to the eye, distending the choriocapillaries and' creating back pressure on the "aqueous veins" which drain the canal of Schlemm. The highest intraocular pressures have been measured under conditions of venous obstruction such as coughing and blowing hard against a mercury column. Inflating a cuff around the neck to 40 torr can double the intraocular pressure. EFFECT OF CENTRAL NERVOUS SYSTEM DEPRESSANTS Whether used for premedication or for the production of anesthesia, most central nervous system depressants-including hypnotics, tranquillizers, neuroleptic agents, and narcotics-probably tend to lower intraocular pressure. A notable exception is ketamine.5 After various preanesthetic medications, which themselves lowered intraocular pressure, I mg./lb. of body weight of this "dissociative" anesthetic given intravenously produced a moderate but statistically significant increase in intraocular pressure to levels above those of controls. A possible explanation for this effect is that ketamine, like succinylcholine, increases the tone of the extraocular muscles. Tonometric values obtained during anesthesia induced by ketamine in more than soo children and infants reflected the intraocular tension found in awake subjects more accurately than those obtained with conventional anesthetics. This is because the reduction in intraocular pressure caused by conventional anesthetics is greater than the increase caused by ketamine. With ketamine, however, diplopia may persist up to 30 minutes during the recovery phase, causing anxiety and apprehension in younger patients.6 Vol. 51, No. 3, March 1975

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OTHER PARENTERALLY ADMINISTERED DRUGS Barbiturates lower intraocular pressure in animals and humans.7' 8 Since the diencephalon influences intraocular pressure,9' 10 central-nervous-system depressants such as barbiturates acting at this site may be expected to influence intraocular pressure." The fall in intraocular pressure produced by barbiturates is due in part to increased facility of aqueous outflow"8 11 and not related to the rate at which aqueous is formed or to changes in blood pressure. Some of the depression of intraocular pressure may be caused by relaxation of the extraocular

muscles.'2 NARCOTICS Morphine administered intramuscularly produces slight ocular hypotension in both normal and glaucomatous eyes.13 Controlled studies of the effects of other narcotics on intraocular pressure have not been published. NEUROLEPTANESTHESIA Induction of anesthesia with Innovar, which contains 2.5 mg. droperidol, a tranquillizer, and 0.5 mg. fentanyl, a narcotic, per milliliter, usually results in moderate decrease in intraocular pressure; however, the eyeballs tend to deviate upward and this causes difficulty in the recording of pressure.'4 Atropine or scopolamine is commonly administered prior to general anesthesia in order to decrease secretions of the upper respiratory tract, to decrease irritability, and to relax smooth muscles. The drug causes a slight transient fall in intraocular pressure in normal eyes. This effect is probably caused by relaxation of smooth muscles.2 In patients with wide-angle glaucoma, scopolamine or atropine in amounts up to o.6 mg. can be given intramuscularly without significant rise in intraocular pressure. Despite this, in glaucomatous patients, preoperative and postoperative instillation of a miotic such as I to 2% pilocarpine into the conjunctional sac have been recommended.15 Although it has been stated frequently that patients with glaucoma should not be premedicated with atropine for fear of precipitating acute glaucoma or aggravating existing chronic glaucoma, these dangers are probably mythical.'6 Assuming uniform distribution of 0.4 mg. of Bull. N. Y. Acad. Med.

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atropine in a 70-kg. patient, the amount of this drug that would be present in the entire eye would be only about o.oooi mg. In contrast, when one drop of i % atropine is instilled into the conjunctival sac, a sizable fraction of the o.6 mg. atropine so administered is probably absorbed into the eye. INHALATION ANESTHETICS All inhalation anesthetics can lower intraocular pressure. Nitrous oxide anesthesia produces intraocular hypotension.1- Moderate to deep anesthesia with ether7' 17 and cyclopropane17 decreases intraocular pressure. This decreased pressure has been attributed to increased facility of aqueous outflow.17 The nonflammable anesthetics-chloroform, halothane, trichlorethylene,18 and methoxyfluorane14 19_-produce equally great depression of intraocular pressure, proportional to the depth of anesthesia. During deep anesthesia with any inhalation anesthetic, the intraocular pressure approaches a common value of 8 to Io torr. MUSCLE RELAXANTS

d-Tubocurarine. As previously mentioned, relaxation of the extraocular muscles by d-tubocurarine also lowers intraocular pressure. At one time the intravenous administration of small increments of d-tubocurarine was advocated in patients undergoing ocular operations under local anesthesia.?° 21 This technique of akinesia by means of curare was reputed to produce relaxation of the lids and extraocular muscles, minimizing the likelihood of extrusion of intraocular contents during cataract operations performed under local anesthesia. The fear that respiratory insufficiency may develop when akinesia is induced by curare has prevented this technique from gaining popularity. Gallamine. With gallamine triethiodide tension remained unchanged during apnea but rose after intubation in more than half of the cases in one study.22 When topical analgesia of the larynx was performed before endotracheal intubation, intraocular pressure usually remained constant or showed a slight fall after gallamine was administered. When other muscle relaxants are used to facilitate endotracheal intubation, prior topical anesthesia of the larynx will probably lessen any increases in intraocular pressure. Succinyicholine. In contrast to d-tubocurarine, succinylcholine chloVol. 51, No. 3, March 1975

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ride elevates intraocular pressure. In 1952 it was demonstrated that succinylcholine and decamethonium produce contracture of the extraocular muscles in rabbits.29 The following year the increase in intraocular pressure after administration of succinylcholine in man was described. This study24 was made on conscious volunteers who described an orbital pressure sensation, vertigo, and diplopia after succinylcholine. Succinylcholine caused a smaller rise in patients under deep anesthesia or had no effect.26 The investigators suggested that the rise in intraocular pressure after succinylcholine is secondary to contraction or contracture of the extraocular muscles. This opinion was based on the finding that the eye tends to rotate away from a severed muscle. A specific microscopic structure now called Felderstruktur has been found in extraocular muscles.25 Unlike other skeletal fibers, these muscles contain large numbers of muscle fibers which, when exposed to stimuli of acetylcholine or immersed in depolarizing solutions, respond with slow tonic contraction. At one time it was recommended that succinylcholine chloride always be used with caution in intraocular operations.26 This opinion was endorsed in a report of loss of vitreous during cataract surgery under light anesthesia. The patient received succinylcholine after the sclera had been incised and the anterior chamber was open.27 It would be expected that drugs which abolish the fasciculations produced by succinylcholine might also prevent the rise in intraocular pressure. Recent studies of this problem"' 29 suggest that hexafluorenium and nondepolarizing mucle relaxants under certain circumstances can inhibit increases in intraocular pressure induced by succinylcholine. The prior administration of the carbonic anhydrase inhibitor acetazolamide30 and the Pl-adrenergic blocking agent propranalolPl also prevent this induced intraocular hypertension. In the last decade it has become increasingly evident that, under normal circumstances, the rise in intraocular pressure which follows the administration of succinylcholine is dissipated before the surgical

operation begins.

Recently the time course of the intraocular hypertensive action of succinylcholine was studied in anesthetized patients with normal eyes.32 The peak action was noted between the second and fourth minutes after the administration of succinylcholine; it subsided by the sixth minute after administration of the drug. Endotracheal intubation Bull. N. Y. Acad. Med.

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exaggerated the intraocular hypertensive effect but did not prolong it. An unusual response to succinylcholine has been reported:33 namely, subacute glaucoma in a patient with an atypical plasma cholinesterase which resulted in prolonged neuromuscular block. SUMMARY

Numerous surgical and anesthetic factors can affect intraocular pressure during ocular operations. An understanding of the physiology of intraocular pressure and of the ways in which it may be altered in the course of an ophthalmological operation is obviously of paramount importance in this area of surgical endeavor. Any interference with venous return from the eye, as is caused by coughing or straining, will interfere with efflux of aqueous and hence will lead to sudden and dangerous increases in intraocular pressure. Fortuitously, all depressants of the central nervous system and all general anesthetics decrease intraocular pressure in proportion to the depth of anesthesia. The only exception to this rule is ketamine. Since the ketamine-induced rise of intraocular pressure is less than the decrease caused by other general anesthetics, this drug is useful in children to facilitate examinations of the eye, including tonometry. Of the neuromuscular blocking agents, succinylcholine has been studied extensively because of its tendency to increase intraocular pressure. Despite this effect there are few ocular contraindications to its use. It should not be used in penetrating wounds of the eye nor administered for the first time once the eye has been opened. Atropine and scopolamine can be used safely for premedication in glaucomatous patients, provided a miotic is instilled into the conjunctival sac. REFER ENCES on intraocular pressure during anesthesia. Anesth. Anaig. (Cleveland) 4g:232, 1963. 4. Bain, W. S. E. and Maurice, D. M.: Physiological variations in the intraocular pressure. Trans. Ophthal. Soc. U.K. 79:249, 1959. 5. Corssen, G. and Hoy, J. E.: A new parenteral anesthetic C1-581: Its effect on intraocular pressure. J. Pediat. Ophthal. 4:20, 1967.

1. Agarwal, L. P. and Mathur, S. P.: Curare in ocular surgery. Brit. J. Ophthal. 36:603, 1952. 2. Colle, J., Duke-Elder, P. M., and DukeElder, W. S.: Studies on the intraocular pressure: I. The action of drugs on the vascular and muscular factors controlling the intraocular pressure. J. Physioi. (London) 71:1, 1931. 3. Duncalf, D. and Weitzner, S. W.: The influence of ventilation and hypercapnia

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6. Corssen, G., Miyasaka, M., and Domino, E. F.: Changing concepts in pain control during surgery: Dissociative anesthesia with C1-581. Anesth. Anaig. (Cleveland) 47:746, 1968. 7. Kornblueth, W., Aladjemoff, L., Magora, F., and Gabbay, A.: Influence of general anesthesia on intraocular pressure in man: The effect of diethyl ether, cyclopropane, vinyl ether and thiopental sodium. Arch. Ophthal. (Chicago) 61: 84, 1959. 8. Stone, H. H. and Prijot, E. L.: The effect of a barbiturate and paraldehyde on aqueous humor dynamics in rabbit. Arch. Ophthal. (Chicago) 54:834, 1955. 9. Lowenstein, O.: Diencphale et glaucome primitif. Ann. Oculist. (Paris) 188:62, 1955. 10. Von Sallmann, L. and Lowenstein, O.: Responses of intraocular pressure, blood pressure and cutaneous vessels to electric stimulation in the diencephalon. Amer. J. Ophthal. 39:11, 1955. 11. deRoetth, A., Jr., and Schwartz, H.: Aqueous humor dynamics in glaucoma: Effect of ganglionic blocking agents and thiopental sodium (Pentothal) anesthesia on aqueous humor dynamics. Arch. Ophthal. (Chicago) 55:755, 1956. 12. Volpi, V. and Mangiavacchi, E.: Richerche sull' ipotonia oculare da anestesia generate con curaro. Ann. Ottal. 84:93, 1958. 13. Leopold, I. H.: Effect of intramuscular administration of morphine, atropine, scopolamine and neostigmine on the human eye. Arch. Ophthal. (Chicago) 40:285, 1948. 14. Ivankovic, A. D. and Lowe, H. J.: The influence of methoxyflurane and neuroleptanesthesia on intraocular pressure in man. Anesth. Anaig. (Cleveland) 48:933, 1969. 15. Schwartz, H., deRoetth, A. Jr., and Papper, E. M.: Preanesthetic use of atropine and scopolamine in patients with glaucoma. J.A.M.A. 165:144, 1957. 16. Rosen, D. A.: Anaesthesia in ophthalmology. Canad. Anaesth. Soc. J. 9:545, 1962. 17. Couadau, A. and Campau, L.: Action de la narcose, du curare et des ganglio-

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plegiques sur la tension du globe oculaire. Arch. Ophthaal. (Paris) 12:287, 1952. Magora, F. and Collins, V. J.: The influence of general anesthetic agents on intraocular pressure in man: The effect of common nonexplosive agents. Arch. Ophthal. (Chicago) 66:806, 1962. Schettini, A., Owre, E. S., and Fink, A. I.: Effect of methoxyflurane on intraocular pressure. Canad. Anaesth. Soc. J. 15:172, 1968. Barraquer, J. I.: El curare en cirugia ocular: Estudios e informaciones oftalmol6gicas. Inst. Barraquer (Barcelona) 2:1, 1949. Kirby D. B.: Use of curare in cataract surgery. Arch. Ophthal. (Chicago) 43: 678, 1950. Goldsmith, E.: An evaluation of succinylcholine and gallamine as muscle relaxants in relation to intraocular tension. Anesth. Anaig. (Cleveland) 40: 557, 1967. Hofmann, H. and Lembeck, F.: Das Verhalten der iussere Augenmuskeln gegenuber Curare, Dekamethonium (C 10) und Succinylcholin (M 115). Nauyn Schmeideberg Arch. Pharm. Exp. Path. 216:552, 1952. Hofmann, H., Holzer, H., Bock, J., and Spath, F.: Die Wirkung von Muskelrelaxantien auf den intraokularen Druck. Klin. Mbl. Augenheilk. 123:1, 1953. Siebeck, R. and Kruger, P.: Die histologische Struktur der ausseren Augenmuskeln als Ausdruck ihrer Funktion. Van Graefe Arch. Ophthal. 156:637, 1955. Lincoff, H. A., Ellis, C. H., DeVoe, A. G., DeBeer, E. J., Impastato D. J., Berg, S., Orkin, L., and Magda H.: Effect of succinylcholine in intraocular pressure. Amer. J. Ophthal. 40:501, 1955. Dillon, J. B., Sabawala, P., Taylor, D. B., and Gunter, R.: Action of succinylcholine on extraocular muscles and intraocular pressure. Anesthesiology 18: 44, 1957. Katz, R. L., Eakins, A. E., and Lord, C. O.: The effects of hexafluorenium in

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preventing the increase in intraocular pressure produced by succinylcholine. Anesthesiology 29:70, 1968. 29. Miller, R. D., Way, W. L., and Hickey, R. F.: Inhibition of succinylchclineinduced increase in intraocular pressure produced by succinylcholine. Anesthesiology 29:70, 1968. o30. Carballo, A. S.: Succinylcholine and acetazolamide (Diamox) in anaesthesia for ocular surgery. Canad. Anaesth.

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Soc. J. 1.2:486, 1965. 31. Kaufman, L.: General anaesthesia in ophthalmology. Proc. Roy. Soc. Med. 60:1280, 1967. 32. Pandey, K., Badola, R. P., and Kumar, S.: Time course of intraocular hypertension produced by suxamethonium. Brit. J. Anaesth. 441:191, 1972. 33. Hains, J.: Glaucoma associated with suxamnethonium apnoea. Anaesthesia 23: 438, 1968.