1072
ANESTH ANALG 1992;75:1070-5
LE’ITERS TO THE EDITOR
Another case report of interest was that of Shantha and Mani (3) in which a sterile Tuohy needle was passed over the epidural catheter and advanced to the epidural space, after which the Tuohy needle and lodged catheter were pulled out together. Although this method was carried out successfully, it has the obvious danger of possibly shearing the catheter and compounding the problem. I have found on occasion when extreme flexion in the lateral decubitus position was not adequate to facilitate removal of the epidural catheter, that rapidly injecting sterile saline, while at the same time exerting steady traction on the epidural catheter with the patient in the flexed position, enabled removal of the catheter. It would appear that increasing the turgor of the catheter by continuously filling it with saline, plus lubricating the surroundings of the catheter with the saline, allows the catheter to be released with greater ease. I hope that this simple technique will be of some clinical value to anesthesiologists who encounter the problem of trapped epidural catheters. Farida Gadalla, MD Department of Anesthesiology The New York HospitallCornell Medical Center 525 East 68th Street New York, NY 10021
References 1. Sia-Kho E, Kudlak T. How to dislodge a severely trapped epidural
catheter. Anesth Analg 1992;74933. 2. Blackshear RH, Gravenstein N, Radson E. Tension applied to lumbar epidural catheter during removal is much greater with patients sitting versus lying (abstract). Anesthesiology 1991;75:A833. 3. Shantha TR, Mani M. A simple method to retrieve irretrivable epidural catheters. Anesth Analg 1991;73:50&9.
Cyclosporine A and Cardiopulmonary Bypass To the Editor: In a recent case report, Eide and Beflenker (1) described reduced cyclosporine A (CsA) levels with the initiation of cardiopulmonary bypass (CPB). The patient was receiving CsA for 5 yr after renal transplant. We observed similar changes in CsA levels with the initiation of CPB in a patient who underwent CPB surgery 14 mo after liver transplantation and present the data to underscore the role of hemodilution. The patient, a 56-yr-old, 78-kg man, received CsA (175 mg every 12 h), along with azathioprine (150 mg every day), and prednisone (10 mg every day) for immunosuppression. Plasma CsA levels on the 3 days before surgery were 290, 307, and 275 ngImL, respectively, on his usual oral dose of CsA. On the morning of surgery, he received oral CsA (175 mg) 6 h before the start of the procedure. Each CsA sample consisted of 4 mL of blood taken from the radial artery catheter and immediately analyzed using a fluorescent immunoassay of a monoclonal antibody to CsA. This technique measures total CsA and does not measure the metabolites. The specificity and sensitivity of this method is >95% and 95%, respectively.
Table 1. Changes in Blood Cyclosporine A Concentration During the Pericardiopulmonary Bypass Time Before CPB (min) 135
CsA (ng/mL) Temp (“C) Hct (%)
90
553 406 35 35 39 35
During CPB (min)
After CPB (min) 3
30
1
14
24
30
295 35 33
259
225 30 18
216 240 223 30 35.2 35.6 18 18 26
28 18
CI’B, cardiopulmonary bypass; CsA, cyclosporine A; Temp, temperature; Hct, hematocrit.
In the operating room, CsA samples were drawn before, during, and after bypass. The CsA levels, along with the corresponding temperatures and hematocrits, are shown in Table 1. In our patient, as in the previous report, CsA levels decreased in the prebypass period. There was a further reduction in the CsA levels with the initiation of CPB. The CsA levels remained decreased during the postbypass period (Table 1). Although there are many factors that may alter the pharmacokinetics of a drug, factors uniquely associated with CPB are dilution of red blood cells and plasma proteins via the pump priming volume, hypothermia, and binding to the bypass circuit on membrane oxygenator. Most evidence suggests that the latter two do not appear to be important (2,3). The most likely explanation for the decreases in CsA noted is hemodilution because this would explain the reduced CsA levels before, during, and after bypass. The major contribution to the dilution of course is the pump prime, which in our case consisted of 2500 mL of plasmalyte A, 100 mL of 25% albumin, and heparin (7300 U), although the 1100 mL of crystalloid administered before CPB accounted in part for the decrease before bypass along with continued metabolism. Nevertheless, because chronic administration of CsA results in accumulation of tissue stores in the peripheral compartment (3), it is unlikely that the decreased levels seen intraoperatively in patients on such chronic CsA therapy are clinically significant, and the intraoperative monitoring of CsA levels may not be useful. More important, although these decreases are noted in two patients who underwent CPB, this decrease in CsA levels and hemodilution can occur in many other patients not undergoing CPB if a large amount of volume of either blood or cystalloid is administered. Such patients receiving short-term therapy may experience an acute lowering of CsA levels, which may affect organ survival. Elliott F. Williams, MD Carol L. Lake, MD Department of Anesthesiology University of Virginia Health Sciences Center, Box 238 Charlottesville, V A 22908
References 1. Eide TR, Beflenker S. Effect of cardiopulmonary bypass on plasma cyclospoM A levels in a renal transplant patient. Anesth Analg 1992;74: 2 8 ~ 0 .
LETTERS TO THE EDITOR
ANESTH ANALG 1992;75:1070-5
2. Burkle WS. Cyclosporine pharmacokinetics and blood level monitoring. Drug Intel Clin Pharm 1985;19101-5. 3. Cohen DJ, Cohen DJ, Loertscher R, et al. Cydosporine: a new immunosuppressive agent for organ hansplantation. Ann Intern Med 1984;lOl: 667-82.
Touchscreen Technology: Potential Source of Cross-Infections To the Editor: Documented cross-infection by contaminated anesthesia equipment is relatively rare. There is no agreement on how much sterilization should be attempted between cases, but most would agree that meticulous cleaning of the nondisposable components of the anesthesia machinery is imperative after use in patients suspected of harboring an infectious organism (1). The introduction of touchscreen technology, demanding more hands-on contact with the anesthesia machine and equipment (2,3), may have increased the possibility for cross-infections in the operating room. These potentially contaminated surfaces represent an expansion of the interaction among the patient, the anesthesiologist, and the machinery. If neglected and not properly cleaned, they can potentially become the source of infections. These surfaces of some modern anesthesia equipment may be regarded as just a monitor and not as a frequently touched control surface. Consequently, these superficies may not be properly disinfected after each case to prevent cross-contamination. It is recommended that one refer to the manufacturer’s cleaning instructions for disinfection, because these surfaces may be damaged by certain chemicals. Given the fact that immunosuppressed patients are increasingly undergoing surgical procedures (4), it is prudent to assume that only the best disinfection and sterilization standards will control the spread of disease. Harold Arkoff, MD Rafael A. Ortega, MD Boston University Medical Center 88 East Newton Street Boston, M A 02118
References 1. Dorsch JA, Dorsch SE. Understanding anesthesia equipment: conshuction, care and complications. 2nd ed. Baltimore: Williams & Wilkins, 1984:415. 2. Bjoraker DG. The Ohmeda 5250 respiratory gas monitor. Anesthesiol Rev 1990;174&&. 3. King PH, Smith BE. An IBM based monitoring system with touchscreen input. Int J Clin Monit Cornput 19907107-11. 4. Greene ER. Acquired inmunodeficiency syndrome: an overview for anesthesiologists. Anesth Analg 1986;651054-8.
Unexpected Results: Consider a Medication Error To the Editor: McLean et al. (1)report the failure of negative aspiration, a test dose with epinephrine, a test done with 100 pg of
1073
fentanyl, and fractionation of the local anesthetic dose in detecting migration into a vein by an epidural catheter that had been working well for 4 h previously. Their evidence for intravascular injection is a seizure after 18 mL of 2% lidocaine with 1:200,000 epinephrine administered over 12 min. The seizure developed 2 min after the last dose of local anesthetic was administered via the catheter. If this was indeed a case of catheter migration, it would be highly unusual. Four usually successful methods of detecting intravascular injection would have failed in the same patient, including the administration of 90 pg of epinephrine intravenously without a significant change in heart rate and 100 pg of fentanyl that had no effect on sensorium. In addition, the 2-min delay in the onset of a seizure after the last fractionated dose and the very modest dose of lidocaine administered allow one to consider other plausible causes for this clinical picture. I believe that the course of events depicted may best be explained by a medication error. Physician-prepared lidocaine (pH adjusted) and multiple test doses with different agents give ample opportunity for error. Succinylcholine was present in the operating room and was used when this patient was urgently converted to a general anesthetic. Medication errors with epidural catheters do occur. There is a long list of medications that have erroneously been injected into the epidural space (2-4). The events in this case presentation are consistent with an epidural injection of succinylcholine. I have heard the exact words that this patient uttered before ”seizing” in a patient given 10 mg of succinylcholine when awake (“What’s happening to me?”). Although this patient‘s adverse result could have been related to an overdose of intravenous lidocaine, I believe that a medication error must also be considered and would recommend that this be part of any differential diagnosis where a drug does not perform as expected. Scott B. Groudine, MD Department of Anesthesiology, A-131 Albany Medical College Albany, NY 12208
References 1. McLean BY, Rottman RL, Kotelko DM. Failure of multiple test doses and techniques to detect inhavascular migration of an epidural catheter. Anesth Analg 1992;74:454-6. 2. Bickler P, Spears R, McKay W. Inhalipid solution mistakenly infused into the epidural space (letter). Anesth Analg 1990;71:712-3 3. JunejaMIvl, Ackerman WE, Bellinger K. Prevention of accidental injection of drugs in epidural tubing. J Post Anesth Nurs 1991;6:28%9. 4. Goodchild CS, Gent JP, Marks RL, et al. Inadvertent epidural midazolam and fentanyl (letter). Anaesthesia 1989;44:609-10.
In Response: Thank you for the opportunity to respond to Dr. Groudine’s letter. I disagree with his conclusion that the case report (1) may be best explained by a medication error. Dr. Groudine believes that the events in our case presentation are consistent with an epidural injection of SUCcinylcholine, in part because he heard an awake patient given 10 mg of succinylcholine say the exact words that our patient used before “seizing.” Dr. Groudine did not mention by what route the succinylcholine was administered to
ANESTH ANALG 1992;75:1070-5
LE’ITERS TO THE EDITOR
Another case report of interest was that of Shantha and Mani (3) in which a sterile Tuohy needle was passed over the epidural catheter and advanced to the epidural space, after which the Tuohy needle and lodged catheter were pulled out together. Although this method was carried out successfully, it has the obvious danger of possibly shearing the catheter and compounding the problem. I have found on occasion when extreme flexion in the lateral decubitus position was not adequate to facilitate removal of the epidural catheter, that rapidly injecting sterile saline, while at the same time exerting steady traction on the epidural catheter with the patient in the flexed position, enabled removal of the catheter. It would appear that increasing the turgor of the catheter by continuously filling it with saline, plus lubricating the surroundings of the catheter with the saline, allows the catheter to be released with greater ease. I hope that this simple technique will be of some clinical value to anesthesiologists who encounter the problem of trapped epidural catheters. Farida Gadalla, MD Department of Anesthesiology The New York HospitallCornell Medical Center 525 East 68th Street New York, NY 10021
References 1. Sia-Kho E, Kudlak T. How to dislodge a severely trapped epidural
catheter. Anesth Analg 1992;74933. 2. Blackshear RH, Gravenstein N, Radson E. Tension applied to lumbar epidural catheter during removal is much greater with patients sitting versus lying (abstract). Anesthesiology 1991;75:A833. 3. Shantha TR, Mani M. A simple method to retrieve irretrivable epidural catheters. Anesth Analg 1991;73:50&9.
Cyclosporine A and Cardiopulmonary Bypass To the Editor: In a recent case report, Eide and Beflenker (1) described reduced cyclosporine A (CsA) levels with the initiation of cardiopulmonary bypass (CPB). The patient was receiving CsA for 5 yr after renal transplant. We observed similar changes in CsA levels with the initiation of CPB in a patient who underwent CPB surgery 14 mo after liver transplantation and present the data to underscore the role of hemodilution. The patient, a 56-yr-old, 78-kg man, received CsA (175 mg every 12 h), along with azathioprine (150 mg every day), and prednisone (10 mg every day) for immunosuppression. Plasma CsA levels on the 3 days before surgery were 290, 307, and 275 ngImL, respectively, on his usual oral dose of CsA. On the morning of surgery, he received oral CsA (175 mg) 6 h before the start of the procedure. Each CsA sample consisted of 4 mL of blood taken from the radial artery catheter and immediately analyzed using a fluorescent immunoassay of a monoclonal antibody to CsA. This technique measures total CsA and does not measure the metabolites. The specificity and sensitivity of this method is >95% and 95%, respectively.
Table 1. Changes in Blood Cyclosporine A Concentration During the Pericardiopulmonary Bypass Time Before CPB (min) 135
CsA (ng/mL) Temp (“C) Hct (%)
90
553 406 35 35 39 35
During CPB (min)
After CPB (min) 3
30
1
14
24
30
295 35 33
259
225 30 18
216 240 223 30 35.2 35.6 18 18 26
28 18
CI’B, cardiopulmonary bypass; CsA, cyclosporine A; Temp, temperature; Hct, hematocrit.
In the operating room, CsA samples were drawn before, during, and after bypass. The CsA levels, along with the corresponding temperatures and hematocrits, are shown in Table 1. In our patient, as in the previous report, CsA levels decreased in the prebypass period. There was a further reduction in the CsA levels with the initiation of CPB. The CsA levels remained decreased during the postbypass period (Table 1). Although there are many factors that may alter the pharmacokinetics of a drug, factors uniquely associated with CPB are dilution of red blood cells and plasma proteins via the pump priming volume, hypothermia, and binding to the bypass circuit on membrane oxygenator. Most evidence suggests that the latter two do not appear to be important (2,3). The most likely explanation for the decreases in CsA noted is hemodilution because this would explain the reduced CsA levels before, during, and after bypass. The major contribution to the dilution of course is the pump prime, which in our case consisted of 2500 mL of plasmalyte A, 100 mL of 25% albumin, and heparin (7300 U), although the 1100 mL of crystalloid administered before CPB accounted in part for the decrease before bypass along with continued metabolism. Nevertheless, because chronic administration of CsA results in accumulation of tissue stores in the peripheral compartment (3), it is unlikely that the decreased levels seen intraoperatively in patients on such chronic CsA therapy are clinically significant, and the intraoperative monitoring of CsA levels may not be useful. More important, although these decreases are noted in two patients who underwent CPB, this decrease in CsA levels and hemodilution can occur in many other patients not undergoing CPB if a large amount of volume of either blood or cystalloid is administered. Such patients receiving short-term therapy may experience an acute lowering of CsA levels, which may affect organ survival. Elliott F. Williams, MD Carol L. Lake, MD Department of Anesthesiology University of Virginia Health Sciences Center, Box 238 Charlottesville, V A 22908
References 1. Eide TR, Beflenker S. Effect of cardiopulmonary bypass on plasma cyclospoM A levels in a renal transplant patient. Anesth Analg 1992;74: 2 8 ~ 0 .
LETTERS TO THE EDITOR
ANESTH ANALG 1992;75:1070-5
2. Burkle WS. Cyclosporine pharmacokinetics and blood level monitoring. Drug Intel Clin Pharm 1985;19101-5. 3. Cohen DJ, Cohen DJ, Loertscher R, et al. Cydosporine: a new immunosuppressive agent for organ hansplantation. Ann Intern Med 1984;lOl: 667-82.
Touchscreen Technology: Potential Source of Cross-Infections To the Editor: Documented cross-infection by contaminated anesthesia equipment is relatively rare. There is no agreement on how much sterilization should be attempted between cases, but most would agree that meticulous cleaning of the nondisposable components of the anesthesia machinery is imperative after use in patients suspected of harboring an infectious organism (1). The introduction of touchscreen technology, demanding more hands-on contact with the anesthesia machine and equipment (2,3), may have increased the possibility for cross-infections in the operating room. These potentially contaminated surfaces represent an expansion of the interaction among the patient, the anesthesiologist, and the machinery. If neglected and not properly cleaned, they can potentially become the source of infections. These surfaces of some modern anesthesia equipment may be regarded as just a monitor and not as a frequently touched control surface. Consequently, these superficies may not be properly disinfected after each case to prevent cross-contamination. It is recommended that one refer to the manufacturer’s cleaning instructions for disinfection, because these surfaces may be damaged by certain chemicals. Given the fact that immunosuppressed patients are increasingly undergoing surgical procedures (4), it is prudent to assume that only the best disinfection and sterilization standards will control the spread of disease. Harold Arkoff, MD Rafael A. Ortega, MD Boston University Medical Center 88 East Newton Street Boston, M A 02118
References 1. Dorsch JA, Dorsch SE. Understanding anesthesia equipment: conshuction, care and complications. 2nd ed. Baltimore: Williams & Wilkins, 1984:415. 2. Bjoraker DG. The Ohmeda 5250 respiratory gas monitor. Anesthesiol Rev 1990;174&&. 3. King PH, Smith BE. An IBM based monitoring system with touchscreen input. Int J Clin Monit Cornput 19907107-11. 4. Greene ER. Acquired inmunodeficiency syndrome: an overview for anesthesiologists. Anesth Analg 1986;651054-8.
Unexpected Results: Consider a Medication Error To the Editor: McLean et al. (1)report the failure of negative aspiration, a test dose with epinephrine, a test done with 100 pg of
1073
fentanyl, and fractionation of the local anesthetic dose in detecting migration into a vein by an epidural catheter that had been working well for 4 h previously. Their evidence for intravascular injection is a seizure after 18 mL of 2% lidocaine with 1:200,000 epinephrine administered over 12 min. The seizure developed 2 min after the last dose of local anesthetic was administered via the catheter. If this was indeed a case of catheter migration, it would be highly unusual. Four usually successful methods of detecting intravascular injection would have failed in the same patient, including the administration of 90 pg of epinephrine intravenously without a significant change in heart rate and 100 pg of fentanyl that had no effect on sensorium. In addition, the 2-min delay in the onset of a seizure after the last fractionated dose and the very modest dose of lidocaine administered allow one to consider other plausible causes for this clinical picture. I believe that the course of events depicted may best be explained by a medication error. Physician-prepared lidocaine (pH adjusted) and multiple test doses with different agents give ample opportunity for error. Succinylcholine was present in the operating room and was used when this patient was urgently converted to a general anesthetic. Medication errors with epidural catheters do occur. There is a long list of medications that have erroneously been injected into the epidural space (2-4). The events in this case presentation are consistent with an epidural injection of succinylcholine. I have heard the exact words that this patient uttered before ”seizing” in a patient given 10 mg of succinylcholine when awake (“What’s happening to me?”). Although this patient‘s adverse result could have been related to an overdose of intravenous lidocaine, I believe that a medication error must also be considered and would recommend that this be part of any differential diagnosis where a drug does not perform as expected. Scott B. Groudine, MD Department of Anesthesiology, A-131 Albany Medical College Albany, NY 12208
References 1. McLean BY, Rottman RL, Kotelko DM. Failure of multiple test doses and techniques to detect inhavascular migration of an epidural catheter. Anesth Analg 1992;74:454-6. 2. Bickler P, Spears R, McKay W. Inhalipid solution mistakenly infused into the epidural space (letter). Anesth Analg 1990;71:712-3 3. JunejaMIvl, Ackerman WE, Bellinger K. Prevention of accidental injection of drugs in epidural tubing. J Post Anesth Nurs 1991;6:28%9. 4. Goodchild CS, Gent JP, Marks RL, et al. Inadvertent epidural midazolam and fentanyl (letter). Anaesthesia 1989;44:609-10.
In Response: Thank you for the opportunity to respond to Dr. Groudine’s letter. I disagree with his conclusion that the case report (1) may be best explained by a medication error. Dr. Groudine believes that the events in our case presentation are consistent with an epidural injection of SUCcinylcholine, in part because he heard an awake patient given 10 mg of succinylcholine say the exact words that our patient used before “seizing.” Dr. Groudine did not mention by what route the succinylcholine was administered to
