Letters to the Editor

Propofol in Cardiac Catheterization To the Editor: We read with interest the article by Lebovic et al. (1)on the comparison of propofol versus ketamine for anesthesia in pediatric patients undergoing cardiac Catheterization. We agree that propofol may well be an alternative to ketamine, but we must reemphasize the cautionary note sounded by the authors-propofol is a myocardial depressant (2,3), and it should be used with this side effect borne in mind. Although mentioned in their article, Lebovic et al. (1) did not emphasize that their method of inducing anesthesia with propofol differs substantially from that commonly used in adults or children (4,5). Usually, a dose of 2-2.5 mg/kg of propofol is used and administered over a total of 40-60 s. Lebovic et al. (1) used 0.5-mg/kg increments, a relatively small dose, with each increment administered over 60 s. The hemodynamic effects of this method of administration may differ substantially from when the usual dose is administered more rapidly, as is usually the case. Another point that we feel must be stressed is patient selection: until more data are available, it is probably not only prudent but l o p a l to avoid propofol in critically ill pediatric patients presenting for cardiac catheterization. Larger doses will contribute to alterations in cardiac output, with reversal of shunt flow causing much more significant alterations in cardiorespiratory variables than those described by Lebovic et al. (1). Maurice Lippmann, MD Richard S. Ginsburg, MD Department of Anesthesiology HarborlUCLA Medical Center 1000 West Carson Street Torrance, CA 90509

References I. Lebovic S, Reich DL, Steinberg LG, Vela FP, Silvay G . Comparison of propofol versus ketamine for anesthesia in pediatric patients undergoing cardiac catheterization. Anesth Analg 1992;74:49M. 2. Lippmann ML, Paicus R, Gingerich S, Owens R, Mok M, Appel P. A controlled study of the hemodynamic effects of propofol versus thiopental during anesthesia induction. Semin Anesth 1988;7(1[Suppll, March]): 116-22. 3. White PF. Propofol: pharmacokinetics and pharmacodynamics. Semin Anesth 1988;7(1 [Suppl 1, March]):P20. 4. Martin LD, Pastemak LR, Pudimat MA. Total intravenous anesthesia with propofol in pediatric patients outside the operating room. Anesth Analg 1992;74:609-12. 5 . Henegods L, Rolly G, Versicheler L, Rosseel MT. Propofol combined with nitrous oxide-oxygen for induction and maintenance of anesthesia. Anesthesia 1987;42:36&5.

To the Editor: We read with interest the clinical research report by Lebovic et al. (1) on the usage of propofol as an anesthetic in

01992 by the lntemational Anesthesia Research Society

pediatric patients presenting for cardiac catheterization. The authors indicated that this was the first presentation to describe the use of propofol in pediatric congenital cardiac diseases and further concluded that “propofol anesthesia is a practical alternative for pediatric patients undergoing elective cardiac catheterization and may be preferable to ketamine because of the significantly shorter recovery time.” This recommendation must be qualified before wide application. We would like to address the following two points. First, congenital heart disease is not a single disease but a vast array of anatomic anomalies. Each anomaly is associated with a set of distinctive clinical features. The clinical course and the physiologic responses to different pharmacologic interventions, as well as the homeostatic reflex to various stimuli during the administration of anesthetics, can be extremely diverse. Propofol is known to cause myocardial depression. In the investigation described by Lebovic et al. (l),it was discovered that 7 of 10 patients developed decreased mean arterial pressure after they were given a propofol infusion. In certain congenital heart diseases (e.g., aortic stenosis), a pharmacologically induced decrease in arterial blood pressure can precipitate adverse patient outcome (2). The use of propofol in patients with aortic stenosis must therefore be considered contraindicated. The notion that one anesthetic can be prescribed for a group of diverse cardiac diseases seems imprudent. Second, the demographic data of the patients enrolled in the study mostly matched when age, body weight, arterial blood oxygen saturation range, and duration of catheterization were compared in the two groups (propofol and ketamine). However, the most important clinical feature in patients undergoing cardiac catheterization is not age, body weight, arterial oxygen saturation, or duration of catheterization, but diagnosis. The diagnosis of congenital cardiac defect, unfortunately, did not match in the two groups. For example, three patients in the ketamine group, but none in the propofol group, were diagnosed as having truncus arteriosus. (The number of patients in the study, 10 in each group, is too small for meaningful statistical analysis among the different diagnoses.) In conclusion, we strongly believe that there is no single anesthetic that is ideal for providing sedation for cardiac catheterization. The result of the comparison between propofol and ketamine is probably not valid, because clinical diagnoses between the two groups of patients did not match. Y. James Kao, PhD, MD Richard G. Norton, MD Department of Anesthesiology Texas Tech University Health Sciences Center 3601 4th Street Lubbock, TX 79430

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References 1. Lebovic S, Reich DL, Steinberg LG, Vela FP, Sylvay G. Comparison of propofol versus ketamine for anesthesia in pediatric patients undergoing cardiac catheterization. Anesth Analg 1992;74490-4. 2. Salem MR, Hall SC, Motoyama GK. Anesthesia for thoracic and cardiovascular surgery. In: Motoyama EK, ed. Smiths anesthesia for infants and children. 5th ed. St. Louis: CV Mosby, 1990, Chapter 19.

In Response: The cautionary note sounded by Drs. Lippmann and Ginsburg is appropriate. We would add, however, that only a small fraction of pediatric cardiac catheterization patients would be expected to experience arterial desaturation or hemodynamic decompensation in response to propofol. Obviously, the principle of slowly administering lower doses of depressant anesthetics applies to all patients with cardiac disease, especially those with right-to-left shunting. Drs. Kao and Norton are correct in pointing out that congenital heart disease represents a wide spectrum of anatomic and physiologc abnormalities and that patients with certain lesions may respond adversely to propofol anesthesia. This point was also emphasized in the discussion section of our article and is a point that is well understood by the readership of this journal. However, we disagree with their contention that the presence of three patients with truncus arteriosus in the ketamine group invalidates the results of the study. They could just as easily have argued that there was only one patient with a double-outlet right ventricle in the propofol group. A study of several hundred patients would be necessary to achieve "statistical" equity between the groups. It is not necessary or economical to proceed with such a massive study to prove what is obvious from our limited study. The point of the study is not that propofol should be used in all patients with congenital heart disease; rather, in properly selected patients, it is a satisfactory anesthetic agent with markedly improved recovery characteristics. In reviewing our further experience with propofol in the cardiac catheterization laboratory, it is being used as the primary anesthetic agent in approximately 70% of cases. We currently induce anesthesia using 1-mgkg bolus doses of propofol, which is repeated once if necessary. Our initial infusion rate is 100 pg.kg-'.min-', which is titrated upward or downward as necessary. Anesthesiologists, as well as pediatric cardiologists and postanesthesia care unit staff, are pleased with the recovery characteristics of propofol. It is likely that propofol will be used more commonly in the future, given the current emphasis on ambulatory care. David L. Reich, MD Department of Anesthesiology The Mount Sinai Medical Center One Gustave L. Levy Place New York, NY 10029-6574

Propofol for Radiation Therapy in Small Children To the Editor: We agree with Martin et al. (1)that propofol is an excellent anesthetic for small children with indwelling central lines

undergoing radiation therapy. However, we have found that when propofol is titrated by small bolus doses or continuous infusion, children are able to maintain their natural airway in both the supine and prone positions, and repeated endotracheal intubation can be avoided. A retrospective chart review of a 1-yr period showed that we had used intravenous anesthesia for 153 of the 156 high-voltage radiation therapy procedures for which anesthesia was requested. Propofol was used as the sole anesthetic in 72 cases and in combination with other anesthetics (midazolam, ketamine, droperidol) in 62 cases. In none of these 153 procedures was the trachea intubated. The radiation procedure itself is painless, and only light levels of anesthesia are needed to keep the child motionless. Patients were monitored with a pulse oximeter, electrocardiograph, respiratory inductane monitor, and an automated oscillometer for automatic arterial blood pressure measurement. Monitors were visible through a window in the treatment room. The children were observed indirectly via videocamera when the anesthesiologist left the room for the 3-7 min required for the treatment. Intravenous anesthesia without endotracheal intubation eliminates the need for an anesthesia machine and waste gas scavenging in a remote location and eliminates the risk of laryngeal trauma from repeated instrumentation. Propofol can be titrated to achieve adequate sedation without undue respiratory or cardiovascular depression. When propofol is used alone, recovery is rapid, and patients are alert before transport. Those patients undergoing daily treatments were able to continue normal daily activities and maintain nutrition. As with all potent anesthetics, careful observation and monitoring of the patient are required, and appropriate equipment and supplies must be available for the management of adverse drug effects or reactions. Mary A. Setlock, MD Barbara W. Palmisano, M D Children's Hospital of Wisconsin A nes thes iology-MS 735 P.O. Box 1997 Milwaukee, W l 53201

Reference 1. Martin LD, Pastemak LR, Pudimat MA. Total intravenous anesthesia with propofol in pediatric patients outside the operating room. Anesth Analg 1992;74:609-12.

In Response: We appreciate the interest that Drs. Setlock and Palmisano have shown in our case report with regard to the use of propofol in pediatric patients outside the operating room (1). We agree with them that propofol is an excellent anesthetic for small children undergoing procedures remote from the operating room and that it has several distinct advantages over previously utilized techniques. We also recognize that airway management for these cases is somewhat a matter of preference. However, this decision must be made in the context of the individual institution. As stated in our article, we chose to carefully intubate the tracheas of our patients for several reasons: (a) one patient had to be transported to several different locations for multiple radiologic procedures; (b) our radiologic suites are very distant from the operating room should assistance be

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required; and (c) the patients had to be placed in multiple positions (supine, prone, and lateral). We had no evidence of airway trauma from repeated airway instrumentation when appropriate care was taken. As stated in the article, more experience with this anesthetic technique may demonstrate that oral intubation may not always be necessary. As Drs. Setlock and Palmisano have demonstrated, we also have found that in selected cases, carefully titrated infusions of propofol achieve adequate levels of sedation for these painless procedures and that patients are able to maintain their natural airways. However, each and every procedure must be planned with the particular institution’s personnel, facilities, and limitations in mind. We therefore believe that the method of airway management must be left to the individual anesthesiologist, who clearly has an understanding of the local environment in which he or she is working. L. D. Martin, MD L. R. Pasternak, MD M. A. Pudimat, MD Department of Anesthesiofogy National Naval Medical Center Bethesdu, M D 20614

Reference 1. Martin LD, Pastemak LR, Pudimat MA. Total intravenous anesthesia with propofol in pediahic patients outside the operating room. Anesth Analg 1992;74:609-12.

Myelopathy and Back Pain -Take Heed To the Editor: Two articles in sequential issues of Anesthesia & Analgesia should have alerted anesthesiologists to the fact that local anesthetics are not innocuous drugs (1,Z). However, these articles did not address other issues that anesthesiologists also should be aware of. Rigler et al. (1)state that “Despite its long history, clear guidelines for safe administration of local anesthetics via an indwelling catheter remain to be established.” A review of the most recent textbooks confirms this statement (two contained nothing on the subject and five only a paragraph) (3-9). Evidently, these books reflect the clinical situation, namely, that intermittent-injection spinal anesthesia has been little used or taught during the past 20 yr. Nevertheless, since 1940, both tetracaine and procaine have been used safely in intermittent-injection spinal anesthesia (1016). However, tetracaine was not administered as in the one case cited by Rigler et al. (1).Futhermore, 5% lidocaine in 7.5% glucose or dextrose, which was used in the other three cases cited by Rigler et al. (l),is intended for use in the single-injection technique. Package inserts for this preparation of lidocaine state that “If the technique is properly performed and the needle is properly placed in the subarachnoid space, it shouldn’t be necessary to administer more than one ampule (100 mg)” (17). It contains no statement about plastic tubing (catheter). Finally, one won-

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ders why for spinal anesthesia, intermittent-injection rather than single-injection techniques were used. Compared with the single-injection technique, intermittent injection is fraught with more complications. All four cases cited by Rigler et al. (1)required only a sensory dermatome level to the tenth thoracic dermatome and durations of 1, 2.5, 3, and 3.5 h. A single injection of no more than 10 mg of hyperbaric tetracaine with duration extended by the addition of 0.2 mg of epinephrine (4-5 h) or 5 mg of phenylephrine ( 5 7 h) would have sufficed. Hynson et al. (2) suspected ”local irritation of the muscles and soft tissues” from chloroprocaine. When chloroprocaine was reintroduced for epidural block in 1971, it contained sodium bisulfite, a known tissue irritant (18,19); however, myelopathy from it did not surface until 1980 (20). In 1988, the bisulfite in chloroprocaine was replaced with the chelating (stabilizing) agent disodium ethylenediaminetetraacetate (EDTA) (21). After injection of this stabilizer into the subarachnoid space of rabbits, it was concluded that the investigation “. . . suggested EDTA has neural blocking effects and may cause complications” (22). One wonders what would happen if 20 mL or more was injected unintentionally into the subarachnoid space of patients? Perhaps nothing, but then, time will tell. Nine years (1971-1980) elapsed before myelopathy from chloroprocaine containing sodium bisulfite surfaced. Hopefully, these two articles (1,2) have notified physicians that trespassing clinically with local anesthetics that have not been carefully and thoroughly researched for the techniques for which they are to be used, can result in significant complications. Daniel C. Moore,

MD

Department of Anesthesiology Virginia Mason Clinic 1100 Ninth Avenue Seattle, WA 98111

References 1. Rigler ML, h a s n e r K, Krejcie TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991;72:275-81. 2. Hynson JM, Sessler DI, Glosten B. Back pain in volunteers after epidural anesthesia with chloroprocaine. Anesth Analg 1991;72:253-6. 3. Canon H, Korbon GA, Rowlingsworth JC. Regional anesthesia. Orlando: Grune & Stratton, 1984:42. 4. Raj PP. Handbook of regional anesthesia. New York Churchill Livingstone, 1985:237. 5. Zenz M, Panhans C, Niesel H C, Kreuscher H. Regional anesthesia year book. Chicago: Year Book, 1985. 6. Wildsmith JAW, Armitage EN. Principles and practice of regional anaesthesia. New York Churchill Livingstone 198770. 7. Brown DL, Wedel DJ. Spinal, epidural and caudal anesthesia. In: Miller RD, eds. Anesthesia. 3rd ed. New York: Churchill Livingstone, 1990: 1407. 8. Bridenbaugh PO, Greene NM. Spinal (subarachnoid) neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. 2nd ed. Philadelphia: J.B. Lippincott, 1988:213. 9. Scott DB. Techniques of regional anaesthesia. East Nonvalk, Conn., Appleton & Lange, 1989194. 10. Lemmon WT. A method for continuous spinal anesthesia: a preliminary report. Ann Surg 1940;111:141. 11. Southworth JL, Hingson RA. Conduction anesthesia: clinical studies of G.P. Pitkin. Philadelphia: 1.B. Lippincott, 1946:827. 12. Schuhmacher LF, Eversole UH. The techniques of spinal anesthesia. Anesthesiology 1942;3:630--13. 13. Bonica JJ. The management of pain. Philadelphia: Lea & Febiger, 1953:4857.

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14. Moore DC.Regional block. Springfield, Ill.: Charles C Thomas, 1953:

15. 16.

17. 18. 19. 20.

485-7. Lund PC. Principles and practice of spinal anesthesia. Springfield, Ill.: Charles C Thomas, 1971:377-94. Adriani I. Regional anesthesia: techniques and clinical applications. St. Louis: Warren H. Greene Inc., 19854146. Xylocaine-MPF (lidocaine hydrochloride) injection with glucose 7.5% Astra Pharmaceutical Products, Inc., 1988. 5 1 Lidocaine hydrochloride and 7.5% dextrose injection, USP. Abbott Laboratories, 1989. Physician’s desk reference. Oradell, N.J.: Medical Economics Company, 1971:1348-9. Tainter ML, Throndson AH, Lehman AJ. Local irritation from sodium bisulfite as a preservative in epinephrine solutions. Proc SOCExp Biol Med 1937:36:584-7. Covino BC, M a n GF, Finster M, Zigmond EK. Prolonged sensory/motor deficits following inadvertent spinal anesthesia. Anesth Analg 1980;59: 39-400.

21. Nesacaine (chloroprocaine HCl) injection, Nesacaine-MPF (chloroprocaine HCI) injection for infiltration and nerve block. Astra Pharmaceutical Products, Inc., 1988. Physician’s desk reference. Oradell, N.J.: Medical Economics Company, 1988:619 22. Wang BC, Hiller JM, Simon EJ, et al. Is EDTA harmless in the subarachnoid space? (abstract). Anesthesiology 1989;71:A1142.

In Response: We appreciate Dr. Moore’s comments. As we have previously stated (l),the purpose of our article was to alert clinicians to a potential risk, to suggest an etiology for the four cases of cauda equina syndrome, and to begin to establish guidelines for the safe administration of local anesthetic through an indwelling subarachnoid catheter (2). Dr. Moore agrees that clear guidelines for continuous spinal anesthesia (CSA) do not exist. Nonetheless, he suggests that since 1940, tetracaine and procaine have been used safely for intermittent-injection spinal anesthesia. However, his citation of the literature is incomplete. For example, the cited report by Schuhmacher and Eversole (3) provides only a description of the technique used for CSA at the Lahey Clinic during the late 1930s and early 1940s; it does not report results nor review complications. The citations do not include the subsequent report published 4 yr later by Nicholson and Eversole (4) that did review the Lahey Clinic experience during that same period and documented five cases of neurologic complications among 21,000 tetracaine spinals. Of these five cases, three occurred with a continuous spinal technique, two of which were classified as cauda equina syndrome. (Unfortunately, the report does not indicate the relative number of cases performed with a single-injection or a continuous technique.) Dr. Moore’s references also do not include other reports in which neural injury was associated with CSA performed with procaine or tetracaine (5,6). Furthermore, the relationship between injury and anesthetic agent may not always be appreciated-as we noted in our article, the three cases of severe urinary retention described in Apgar’s (6) series of 422 cases of CSA performed with procaine likely reflect local anesthetic neurotoxicity. Thus, the use of tetracaine or procaine for CSA as described by these early investigators cannot be viewed as entirely safe. In the four cases of cauda equina syndrome reported in our article (2), there was evidence of a focal sensory block, and to achieve adequate anesthesia, a dose of local anesthetic was administered that was greater than that usually used with a single-injection technique. We postulated that

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the combination of maldistribution and a relatively high dose of local anesthetic exposed neural tissue to a toxic concentration of anesthetic. We have been able to demonstrate in a model of the subarachnoid space that when maldistribution occurs, the concentrations achieved with repeated administration of hyperbaric local anesthetic are potentially neurotoxic (7). However, prior to our report of the four cases, concerns with regard to neurotoxicity from high doses of local anesthetic were confined primarily to chloroprocaine (8). The dosages of local anesthetics commonly administered intrathecally have been tailored to achieve an appropriate dermatomal level and duration, not to avoid neurotoxicity. Previous reports of CSA often have commented on the wide variability in anesthetic requirement and suggested, as in the Lemmon (9) article cited by Dr. Moore, that the “dose should be given as needed.” Although the package insert for 5% lidocaine indeed does suggest that 100 mg should be sufficient, it fails to state that this dose should not be exceeded nor caution that neural injury might result. Conversely, higher doses of lidocaine have often been recommended or administered. For example, the textbook by Lund (lo), which Dr. Moore cites, suggests a dose of “100 to 150 (or more) mg for upper abdominal procedures,” whereas Morch et al. (ll), using a catheter technique, administered doses of 150 to 550 mg, with doses as high as 250 mg administered to establish the initial block. Dr. Moore believes that 5% lidocaine in 7.5% dextrose is for use in a single-injection technique, noting that the package insert does not mention administration of the anesthetic through a catheter. This view is inconsistent with his belief that tetracaine and procaine are appropriate for CSA, because neither the insert for procaine (12) nor for tetracaine (13) refers to such use. It is also inconsistent that Dr. Moore cites Lund (10) but fails to acknowledge Lunds conclusion that “Any local anesthetic agent which is suitable for [single-injection] spinal anesthesia may be used for [CSA].” Of note, Morch et al. (ll),one of the first to report 5% lidocaine in 7.5% dextrose to be “a safe, potent and satisfactory agent for spinal anesthesia,” delivered the anesthetic through a catheter. However, a major point in our article was that neurotoxic injury resulted from the combination of maldistribution and a high dose of relatively concentrated local anesthetic. Consequently, we suggested that the lowest effective concentration of local anesthetic be used. This recommendation is based on data indicating that the risk of neurologic injury is, at least in part, concentration dependent (14). If maldistribution occurs, the concentration of local anesthetic will not be adequately diluted by cerebrospinal fluid. Therefore, we recommend that 5% lidocaine not be used-this concentration is in excess of that needed for adequate blockade. We suggest that lower concentrations be selected for single-injection spinal anesthesia as well: the appropriateness of injecting a particular local anesthetic into the subarachnoid space should not be based on whether it is to be administered through a needle or a catheter, nor with a single-injection or a continuous technique, but, rather, the intrinsic characteristics of the anesthetic solution. We also recommended that a test dose should be administered, after which the extent of blockade should be

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assessed; if maldistribution of anesthetic is suspected, maneuvers such as changing patient position, altering the lumbosacral curvature, switching to a different baricity of local anesthetic, or manipulating catheter position should be used; if these maneuvers fail to correct the problem, the technique should be abandoned. We have suggested that similar cautions be applied when repeating single-injection spinals that have failed to provide adequate analgesia (15). Maldistribution can occur with a single-injection technique, and there is the potential (albeit less than with an indwelling catheter) for repeat injections to distribute in the same restricted pattern; this restricted distribution could result in neurotoxic concentrations of local anesthetic-a review of the closed-claim database appears to support these concerns (15). We do not agree with Dr. Moore that, in comparison with a single-injection technique, CSA is fraught with complications. Conversely, the continuous technique offers potential advantages. With CSA, the duration of anesthesia can be controlled by administering incremental doses of short-acting local anesthetics, and there is evidence to suggest that anesthesia can be maintained for extended periods without prolonging recovery. In a preliminary study, we observed that the length of stay in the postanesthesia care unit was unrelated to the duration of the surgical procedure (16). Although the single-injection technique also can provide anesthesia for extended periods (e.g., addition of a vasoconstrictor to tetracaine), the inability to predict anesthetic duration or surgical time accurately can lead to failure of the spinal technique or to prolonged recovery. In addition, CSA allows greater control of the extent of blockade, which, in a preliminary study, has been shown to correlate with hypotension, bradycardia, and nausea and vomiting (17); additional preliminary data suggest that patients receiving a continuous technique have a lower requirement for vasopressors (18). We appreciate and share Dr. Moore's concern that the renaissance in regional anesthesia flourish; and we do hope, as Dr. Moore suggested, that our article will serve to alert clinicians that "local anesthetics are not innocuous drugs." Kenneth Drasner, MD Mark L. figler, MD Department of Anesthesia University of California, Sun Francisco San Francisco, CA 94143-0648

Tom c. Krejcie, MD Sharon J. Yelich, MD Department of Anesthesia Northwestern University Chicago, ZL 6061 1

Faith T. Scholnick, DO Department of Anesthesia Northlake Regional Medical Center Atlanta, G A 30084

James DeFontes, MD David Bohner, CRNA Department of Anesthesia Kaiser Permanente Orange County, CA 92807

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References 1. Drasner K, Rigler M, Krejcie T, et al. Catheter spind anesthesia and cauda equina syndrome: an alternate view (letter). Anesth Analg 1991; 73:369-70. 2. Rigler ML, Drasner K, Krejcie TC, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991;72:27=1. 3. Schuhmacher LF, Eversole UH. The techniques of spinal anesthesia. Anesthesiology 1942;3:63(!43. 4. Nicholson MJ, Eversole UH. Neurological complications of spinal anesthesia. JAMA 1946;132:679435. 5. Kennedy F, Effron A, Perry G. The grave spinal cord paralysis caused by spinal anesthesia. Surg Gynecol Obstet 1950;91:38598. 6. Apgar V. Continuous spinal anesthesia. Anesthesiology 1942;3:522-9. 7. Rigler M, Drasner K. Distribution of catheter-injected local anesthetic in a model of the subarachnoid space. Anesthesiology 1991;75:68492. 8. Covino BG. Toxicity of local anesthetic agents. Acta Anaesthesiolog Belgica 1988:39(Suppl 2):159-64. 9. Lemmon WT. A method for continuous spinal anesthesia: a preliminary report. Ann Surg 1940;111:1414. 10. Lund PC. Principles and practice of spinal anesthesia. Springfield, 111.: Charles C Thomas, 1 9 7 1 : 3 0 W . 11. March ET, Rosenberg MK, Truant AT. Lidocaine for spinal anaesthesia. A study of the concentration in the spinal fluid. Acta Anaesthesiol Scand 1957;1:105-15. 12. Novocaine@(procaine hydrochloride injection, USP). New York: Winthrop Pharmaceuticals, Division of Sterling Drug, Inc. New York: N.Y., 1988. 13. Pontocaine" (tetracaine hydrochloride). New York Winthrop Pharrnaceuticals, Division of Sterling Drug, Inc., 1987. 14. Ready LB, Plumer MH, Haschke RH, Austin E, Sumi SM. Neurotoxicity of intrathecal local anesthetics in rabbits. Anesthesiology 1985;63:364-70. 15. Drasner K, Rigler M. Repeat injection after a "failed spinal'-at times, a potentially unsafe practice (letter). Anesthesiology 1991;75:71W. 16. Drasner K, Connolly M, Reece WM. Continuous spinal anesthesia: use of a 28-gauge catheter threaded through a 22-gauge needle (abstract). Reg Anesth 1990;15(18):34. 17. Carpenter RL, Caplan RA, Brown DL, Nadir B. Preliminary results of the spinal suweillance study (abstract). Reg Anesth 1990;15(15):41. 18. Palas, TAR. Continuous spinal anesthesia versus single shot technique in the elderly (abstract). Reg Anesth 1990;14(2S):9.

Epidural Hematoma: Was Catheter Removed During Complete An ticoagulation? To the Editor:

A recent case report linked the occurrence of an epidural hematoma to the presence of a congenital spinal arteriovenous abnormality (1). However, review of the case presentation raises a basic q u e s t i o n d i d removal of the epidural catheter while the patient was still undergoing anticoagulation therapy result in the epidural hematoma? A 71-yr-old man underwent a carotid endarterectomy under cervical epidural anesthesia. Heparin (5000 U) was administered intravenously. The epidural catheter was removed at the end of the procedure, approximately 120 min after the dose of heparin, without checking coagulation studies. Approximately 30 min later, the patient began complaining of discomfort in the chest, arm, and back. Emergent surgical exploration revealed a cervical epidural hematoma and an "extensive plexus" of veins covering the dura. Coagulation studies were performed approximately 260 min after the heparin dose and were normal.

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Other cases have been reported in which an epidural catheter was removed from a patient undergoing anticoagulation therapy, who went on to develop an epidural hematoma ( 2 4 ) . In one case, heparin (5000 LJ) was administered 70 min before the epidural catheter was removed. At 2 h, a Lee-White clotting time remained elevated (21 min; normal 5-15 min) (3). Recommendations exist with regard to the removal as well as the insertion of epidural catheters. One group recommended "frequent activated clotting time analyses" to ensure neutralization of heparin activity before epidural catheter removal (5). An editorial published in the newsletter of the American Society of Regional Anesthesia stated that one should "leave the epidural catheter in place until all systemic anticoagulation is neutralized or reversed' (6). Therefore, the presence of a congenital spinal arteriovenous abnormality may predispose a patient to an epidural hematoma; but the removal of an epidural catheter when a patient remains in an anticoagulated state will do so as well. An epidural catheter should be left in place until anticoagulation has been corrected. Removal can then be accomplished safely. Donald S. Stevens, MD Acute Pain Management Service University of Massachusetts Medical Center 5.5 Lake Avenue North Worcester, M A 01655

References 1 Eastwood DW. Hematoma after epidural anesthesia: relationship of skin

and spinal angiomas. Anesth Analg 1991;73352-4. 2. Butler AB, Green CD. Hematoma following epidural anaesthesia. Can Anaesth Soc J 1970;176359. 3. Helperin SW, Cohen DD. Hematoma following epidural anesthesia: report of a case. Anesthesiology 1971;35:6414. 4. Janis KM. Epidural hematoma following postoperative epidural analgesia: a case report. Anesth Analg 1972;51:68%92. 5. Stanley TH, Lunn JK. Anticoagulants and continuous epidural anesthesia (letter). Anesth Analg 1980;59:394-5. 6. Johnson MD, Fox J. Anticoagulation and penoperative intraspinal anesthesia. American Society of Regional Anesthesia Newsletter 1987;92-4.

In Response: Dr. Stevens asks a fair question: "was the epidural catheter removed during complete anticoagulation?" There were no clinical signs of excess bleeding or delayed clot formation during the carotid endarterectomy. Blood samples that were obtained at the onset of symptoms did clot. The hematologist found no clotting defects. It remains that this does not rule out continuing anticoagulation activity. The wormlike nest of veins in the epidural space at surgery associated with the hemangioma on the chest wall still remains a possible cause for the hematoma and the reason for the original report. I agree that the coagulation status must be established before removal of the epidural catheter. Douglas W. Eastwood, M D Department of A nesthesioiogy CWRU Schwl of Medicine 2078 Abington Road Cleveland, OH 44106

Long-Distance Anesthesia To the Editor: I should like to agree with Dr. Boyd and coworkers (1) concerning "long-distance anesthesia," which I also use in ophthalmic anesthesia. There may, however, be a problem with standard calculated minute volume (Vmin) and tidal volume (Vt). The anesthetic dead space is from the Y-piece to the tip of the endotracheal tube. There is, however, further effective dead space. This further dead space is in the compliance of the ventilatory tubing. Most tubing in use has a compliance of $5 mL/cm H,O at room temperature (20°C); therefore, with an airway pressure of 20 cm H,O, there is 6C-lo0 mL of fresh gas used in the expansion of the tubing. If the tubing is doubled in length, then the expansion volume rises to 120-200 mL. The Vt measured at the inspiratory or expiratory port of the ventilator will be patient tidal volume plus expansion volume. When measured at the Y-piece, only patient tidal volume is measured. It is possible to measure Vt at the Y-piece by an electronic spirometer or, more easily, by an in-line vane-type or resistance flowmeter. It is therefore important in long-distance anesthesia to either know the compliance of the tubing used or to measure Vt at the Y-piece. Alternatively, end-tidal CO, measured at the Y-piece also confirms adequate alveolar ventilation despite the length of the tubing. For ophthalmic anesthesia, I have been using a closedcircuit anesthesia system with ventilatory tubing 2 m in length (4m overall). This allows full access to the patient's head for surgical purposes. Knowing the compliance of the tubing, I can calculate the actual tidal volume that the patient is receiving. I confirm adequate alveolar ventilation by monitoring end-tidal CO, and hemoglobin 0, saturation. I would agree with Dr. Boyd and coworkers that there appears to be a perception that the patient must be close to the ventilator. However, assuming that all of the above are taken into account, then there is no reason why the ventilator cannot be a reasonable distance from the patient, yet still be in a safe location and provide surgical access. John Dunphy, FFARCSI Department of Anaesthesia Waterford Regional Hospital A rdkeen , Waterford Ireland

Reference 1. Boyd G, Funderburg BJ, Vasonez LO, Guzman-Stein, G . Long-distance

anesthesia. Anesth Analg 1992;74:477.

In Response: We were encouraged by Dr. Dunphy's letter with regard to our article on long-distance anesthesia, which he also utilizes. We certainly concur with his statements about the compliance of the ventilator tubing as a factor in calculating the delivered tidal volume. To compensate, we usually add approximately 100 mL to the estimated tidal volume re-

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quired by the patient. The volume is then adjusted for an end-tidal CO, of 35 mm Hg. Furthermore, the hemoglobin 0, saturation is monitored in every patient. This was an omission on our part, and we appreciate Dr. Dunphy's comments. Gwendolyn L. Boyd, MD B. J. Funderburg, CRNA Luis 0. Vasconez, MD Gabriela Guzman-Stein, MD Departments of Anesthesiology and Surgey UAB School of Medicine 845 Iefferson Tower 619 South 19th Street UAB Station Birmingham, AL 35233-1924

always plastic, and its extremity is blunt. The close fit of the probe and the endotracheal tube is important, because it prevents a foreign body from coming between the probe and the endotracheal tube.

A. Mayne, MD E. Collard, M D P. Randour, MD v. Delire, MD K. Joucken, MD Anesthesiology Service University Clinics of Mont Godinne 5530 Yvoir Belgium

Reference 1. Knuth TE, Richards JR. Mainstem bronchial obstruction secondary to nasotrachealintubation:a case report and review of the literature. Anesth Analg 1991;73:487-9.

An Atraumatic Oral and Nasotracheal Intubation Guide Probe To the Editor: I would like to comment on the case report by Knuth and Richards (1).Tracheal intubation via the nasal approach is not a rare event. In children, nasal intubation is used for amygdalectomy or to adequately fix the endotracheal tube when the child's head is too far from the anesthesiologist. In adult surgery, nasal intubation is performed in otolaryngology-head and neck surgery and in oral and dental surgery. In our university clinic, we always use a tube with a flexible guide probe and a blunt extremity for all oral or nasal endotracheal intubation (Figure 1).This probe, which is well adapted to the endotracheal tube diameter, has two advantages: (a) it facilitates oral intubation without larynx trauma when laryngoscopy is difficult, and it can be used together with the Magill forceps to facilitate intubation; (b) it prevents the inhalation of foreign bodies and keeps anatomic structures (adenoids or turbinate) out of the airway. This probe also prevents insufflation in the airway of an object set in the endotracheal tube. The tube is easy to use and without risk for the patient because the probe is

Figure I. EsophageaI tubes (5, 6, and 8 mm) manufactured by Rush AG, Kemum, Germany.

More on Epidural Fentanyl Analgesia To the Editor: In their discussion of epidural fentanyl analgesia, Glass et al. (1) comment as follows: "Using the epidural route, the concentration and volume of the fentanyl dose as well as the site of the epidural catheter in relation to the site of surgery is important in providing optimal analgesia with the smallest dose." I suggest that volume and concentration are not important. I do believe that epidural placement site is important in providing superior analgesia with smaller doses of fentanyl and wonder why, considering the above statement, Glass et al. decided to place catheters in the low lumbar epidural space. It would have been more appropriate to place the catheters in a low thoracic interspace, because the opiate receptors are found in the spinal cord, which ends at L-2. As residents, anesthesiologists learn epidural therapy using bolus doses of local anesthetic for anesthesia. Now we are using continuous infusions of narcotics for epidural analgesia. One cannot consider these to be equivalent in theory or practice. I believe that a slow, continuous infusion, for example, either 3 mL/h (0.05 mL/min) or 6 mL/h (0.1 mUmin) to administer 60 Pg/h of fentanyl, presents an inconsequential difference of volume to structures in the dynamic epidural space. The argument is that dose is important and concentration (volume) less critical. The finding of an optimal concentration for bolus epidural fentanyl by Welchew (2) does not necessarily apply to a continuous fentanyl infusion. Glass et al. (1) claim that intravenous and epidural fentanyl provide equivalent analgesia when administered by patient control. In their study, catheters were placed in the lumbar epidural space. The epidural space has a large potential volume in the lumbar region compared with the thoracic region. With narcotics administered in the lumbar epidural space, which is dynamic and filled with adipose tissue and blood vessels, one would assume that very little

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if any of the analgesic effect would be neuraxial. The obvious reason is that the epidural structures would distribute lipophilic opioids systemically. Thus, I agree with Glass et al. (1) that intravenous fentanyl is probably equivalent to lumbar epidural fentanyl. Perhaps morphine, which is hydrophilic, is the only opioid appropriate for analgesia with lumbar catheter placement. Nonetheless, I use fentanyl as my drug of choice for epidural analgesia, with catheter placement determined by the dermatomal origin of pain. There is support for this technique by at least one clinical study. In an abstract by Bodily et al. (3), it is reported that fentanyl epidural analgesia for postthoracotomy pain is influenced by the site of epidural catheter placement. Those patients who had lumbar catheters were not as comfortable as those who had thoracic catheters, even though they received 50% more fentanyl. I draw two conclusions: (a) epidural fentanyl provides segmental analgesia; and (b) there is a significant neuraxial component of analgesia with thoracic epidural administration of fentanyl. The Glass et al. (1) research might have confirmed the Bodily et al. (3) study had they placed their catheters appropriately. Lex Hubbard, MD Department of Anesthesiology Schumpert Medical Center 915 Margaret Place P.O. BOX 22976 Shreveport, LA 71120-2976

References 1. Glass PSA, Estok 1', Ginsberg B, Goldberg JS, Sladen RN. Use of patient-controlled analgesia to compare the efficacy of epidural to intravenous fentanyl administration. Anesth Analg 1992;74:34551. 2. Welchew EA. The optimum concentration for epidural fentanyl. A randomized, double-blind comparison with and without 1:200,000 adrenaline. Anaesthesia 1983;38:1037-41. 3. Bodily MN, Chamberlain DI', Ramsey DH, et al. Lumbar versus thoracic epidural catheter for post-thoracotomy analgesia (abstract). Anesthesiology 1989;71:A1146.

To the Editor: Glass et al. (1) presented an interesting approach to postoperative pain management with the use of patientcontrolled administration of fentanyl via the epidural and intravenous routes. However, we believe that their conclusion, that analgesic effects of fentanyl in the epidural space are due to plasma concentrations, is somewhat misleading. In view of the site of infusion, one should not be surprised that the analgesic effect of fentanyl is due primarily to systemic rather than neuraxial antinociceptic activity. An alternative conclusion that one may draw from this study is that for a drug such as fentanyl to be effective, one must place it close to its dermatomal site of desired action. In support of this, and in contrast to Glass et al. (l),we find epidural fentanyl infusions to be very effective in low doses (i.e., 1.0 pg.kg-'.h-') in the control of postoperative pain in patients with upper abdominal and flank incisions. Pharmacokinetic work by Gourlay et al. (2) very clearly defined the potential limitations when using epidural fentanyl for postoperative pain control. Infusions via an L3-4 catheter demonstrated that fentanyl, being very lipophilic, would not diffuse well in a cephalad direction. As a consequence, to achieve good pain control with epidural

fentanyl, one must place it at the appropriate dermatomal level, as Wolfe et al. (3) did and as we do. Opioid activity in the spinal cord is primarily the result of nociceptive inhibition at the dorsal horn level of entry (i.e., for an upper abdominal incision at the T8-10 dermatomal level). One must place a catheter at that level to expect a good result when using highly lipophilic opioids, such as fentanyl, sufentanil, or alfentanil. Our experience with over 600 epidural infusions demonstrates that lowdose fentanylhupivacaine infusions (5 pg/mL and 0.125%, respectively) at rates of 6-12 mL/h give excellent relief for postoperative pain. Patient satisfaction with our continuous infusion technique is very high, especially at night. This technique does not require that patients awaken in pain before giving themselves a dose of analgesic, as would patient-controlled analgesia. In theory, continuous epidural infusions may permit the use of lower doses of narcotics, in part due to the maintenance of steady-state drug concentrations at the dorsal horn. However, patient comfort is the primary goal, not necessarily saving doses of narcotic drugs. In conclusion, we have found epidural infusions to be both highly effective for control of postoperative pain as well as very safe for use on general surgical wards. We offer this as a respectable alternative to the use of epidural patient-controlled analgesia. Bruce D. Nicholson, MD John Rowlingson, MD Department of Anesthesiology University of Virginia Health Sciences Center Box 238 Charlottesville, V A 22908

References 1. Glass FSA, Estok ,'I Ginsberg 8, Goldberg JS, Sladen RN. Use of patient-controlled analgesia to compare the efficacy of epidural to intravenous fentanyl administration. Anesth Analg 1992;74:34551. 2. Gourlay G, Murphy TM, Plummer JL, Kowalski SR, Cherry DA, Cousins MJ. Pharmacokinetics of fentanyl in lumbar and cervical CSF following lumbar epidural and intravenous administration. Pain 1989;38:25>9. 3. Wolfe MJ, Davies GK. Analgesic action of extradural fentanyl. Br J Anaesth 1980;52:357-8.

In Response: Drs. Nicholson and Rowlingson and Dr. Hubbard all raise a very important issue with regard to positioning the epidural catheter when administering epidural fentanyl. It is true that the same principles pertaining to the administration of epidural local anesthetics cannot be extrapolated to the administration of epidural opioids. Local anesthetics act on nerve roots as they pass through the epidural space, whereas opioids have to traverse the dura and cerebrospinal fluid to reach the dorsal horn of the spinal cord to reach their site of action. Because the spinal cord ends at L-1 in the adult, a lumbar epidural catheter at or below this level will increase the distance that the opioid has to traverse, compared with a catheter placed at the thoracic level. The implication is therefore that using an epidural catheter placed at the lumbar level would require a larger dose of fentanyl to provide effective analgesia than an epidural catheter placed over the involved dermatome at the thoracic level. This supposition has not been systematically

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investigated. A recent study did compare lumbar with thoracic epidural administration of fentanyl after thoracic surgery (1). The investigators were unable to show a significant difference between the two routes of administration in either quality of analgesia, dose, or fentanyl plasma concentrations. It is also interesting to note that Drs. Nicholson and Rowlingson recommend an infusion of 30-60 pg/h of fentanyl (in combination with 0.125%bupivacaine). This hourly dose of fentanyl is,the same as that (4c.50 /@h) required intravenously by the patients in our study (2) (as well as others (31) to achieve very satisfactory analgesia. It should also be noted that the less lipid-soluble opioids will tend to migrate cephalad in the cerebrospinal fluid. Therefore when an opioid (especially one like morphine) is administered in the lumbar epidural space, the onset of analgesia may be altered but not the efficacy of the dose. It is common for a physician to insert a lumbar epidural catheter for the administration of local anesthetics intraoperatively and then utilize this same catheter for postoperative pain management. Thus, the results of our study are pertinent for normal clinical practice and enable the clinician in such instances to make a more rational choice as to either the drug (fentanyl vs morphine) or mode of its administration (epidural vs intravenous) that is optimal for patient postoperative pain management. Peter s. A. Glass, MD Brian Ginsberg, MD Robert N. Sladen, MD Department of Anesthesiology Box 3094 Duke University Medical Center Durham, NC 27710

References 1. Coe A, Sarginson R, Smith MW, Donnefly RJ, Russel GN. Pain following thoracotomy. A randomized double-blind comparison of lumbar versus thoracic epidural fentanyl. Anaesthesia 1991;46918-21. 2. Glass PSA, Estok P, Ginsberg 8, Goldberg JS, Sladen RN. Use of patient-controlled analgesia to compare the efficacy of epidural to intravenous fentanyl administration. Anesth Analg 1992;74345-51. 3. Gourlay GK, Kowalski SR, Plummer JL, Cousins MJ, Armstrong PJ. Fentanyl blood-concentration-analgesic response relationship on postoperative pain. Anesth Analg 1988;67329-37.

Malignant Hyperthermia During Sevoflurane Anesthesia

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rate, end-tidal CO,). The relative contribution is difficult to discern. In the second case, we question more strongly the association between sevoflurane administration and MH. Whereas it is not certain whether the malfunction of the vaporizer suspended or overevaporated the isoflurane, the exposure to sevoflurane for only 30 min is not likely to have provoked MH. It has been shown that sevoflurane is a less potent trigger of MH than other volatile anesthetics (3). The late onset of MH by volatile anesthetics must be considered when establishing the etiology of MH (2). Also, lethal MH occurred in this patient, who had a history of general anesthesia without a previous problem. In addition, warm skin or muscle rigidity was not shown, and the ineffectiveness of dantrolene is worthy of notice. Muscle biopsy or a postmortem examination of the hypothalamus (4), or both, would have been informative. These cases are also of interest because of the potential anesthetic interactions that may produce undesirable effects. In our institute, we have used sevoflurane frequently to induce anesthesia in children because of its rapid onset of action. Usually, isoflurane is then used for maintenance of anesthesia. The interactions between these anesthetics and others must therefore be studied, because such combinations may be used, owing to the rapid uptake and elimination of sevoflurane. Hiroshi Otsuka, MD Osamu Kemmotsu, m, PhD, FCCM Department of Anesthesiology Hokkaido University School of Medicine N15 W7 Sapporo 060 Japan

References 1. Ochiai R, Toyoda Y, Nishio I, et al. Possible association of malignant hyperthermia with sevoflurane anesthesia. Anesth Analg 1992;746164. 2. Otsuka H, Komura Y, Mayumi T, Yamamura T, Kemmotsu 0, Mukaida K. Malignant hyperthermia during sevoflurane anesthesia in a child with central core disease. Anesthesiology 1991;75:699-701, 3. Matsui K, Fujioka Y, Kikuchi H, et al. Effects of several volatile anesthetics on the Ca2'-related functions of skinned skeletal muscle fibers from the guinea pig. Hiroshima J Med Sci 1991;40:9-13. 4. Cranston WI. Central mechanisms of fever. Fed Proc Fed Am SOCExp Biol 1979;38:49-51.

Cannulation of Vessels Using a Spring-Loaded Device To the Editor:

To the Editor: We read with interest the article by Ochiai and colleagues (1)describing the possible association between the administration of sevoflurane and the development of malignant hyperthermia (MH). Because of the important implications of such findings, we believe that a critical examination of their case reports is necessary. We agree that sevoflurane may be associated with MH, as we had previously reported (2). In the first case report by Ochiai et al. (l),the findings are consistent with the development of MH; but we also note that impairment of CO, absorption by sevoflurane may also cause several of the findings (e.g., increased heart

Cannulation of blood vessels is an important part of managing seriously ill patients, especially neonates and infants. The procedure requires very fine hand control and considerable practice. Although it is an operation performed many times, it can be a daunting experience for some (1). Intravenous cannulas are designed with an introducer needle that is slightly longer and narrower than the cannula. Difficulties are usually encountered once the vessel has been punctured by the needle, and the cannula is advanced. The needle may bend considerably during insertion, making manipulation difficult (2). Additionally, the needle tip may be accidentally advanced or prematurely withdrawn, resulting in failure.

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2. Kestin I. Peripheral venous cannulae. Br J Hosp Med 1987;37423,46-S. 3. Datta S, Hanning CD. How to insert a peripheral venous cannula. Br J Hosp Med 1990;43:67-9.

Use of Transesophageal Echocardiogram for Intracardiac Thrombus Related to Postoperative Atrial Fibrillation -

Figure 1. (a) Central venous pressure line guide wire used as spring; @) rectangular plastic base; (c) tube to hold the hub of the cannula; (d) “2’-shaped hook; (e) intravenous cannula with wings.

Figure 2. Cannula held with the device spring in tension.

By experiment, I have found that spring-loading the cannula greatly eases this procedure. The spring is put under tension before the vessel is punctured. Once the vessel is punctured, release of the spring pushes the cannula forward in a swift, smooth motion, avoiding the problems normally encountered. The device (Figure 1) is constructed using a central venous pressure line guide wire that acts as a spring. While the cannula is held in place on the needle with a finger on one of the wings, the free ends of the wire are hooked over the near side of each wing (Figure 2). This puts forward pressure on the cannula. The cannula is held with the wire under tension, and the vessel is pierced as usual. Once the needle is within the lumen, signaled by a ”flashback” of blood (3), the resisting finger can be released, and the cannula moves forward into the blood vessel. The spring and the needle are withdrawn, leaving the cannula in situ. This technique was assessed in 50 infants (92%weighing