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Severe maternal bradycardia and asystole after combined spinal-epidural labor analgesia in a morbidly obese parturient
Case Reports Severe Maternal Bradycardia and Asystole after Combined Spinal-Epidural Labor Analgesia in a Morbidly Obese Parturient Peter H. Pan, MD,* Charles H. Moore, PhD,† Vernon H. Ross, MD‡ Department of Anesthesiology, Wake Forest University School of Medicine, WinstonSalem, NC and Department of Anesthesioloy, Medical College of Virginia Health System, Richmond, VA
*Associate Professor of Anesthesiology, Division of Obstetric Anesthesia, Wake Forest University School of Medicine †Adjunct Professor of Anesthesiology, Division of Obstetric Anesthesia, Medical College of Virginia Health System, Richmond, VA ‡Assistant Professor of Anesthesiology, Division of Obstetric Anesthesia, Wake Forest University School of Medicine Address correspondence to Dr. Pan at the Department of Anesthesiology, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA. E-mail: [email protected] Presented in part as a poster at the annual meeting for the Society of Obstetric Anesthesia and Perinatology, Hilton Head, SC, May 2002. Received for publication August 6, 2003; revised manuscript accepted for publication October 28, 2003. Journal of Clinical Anesthesia 16:461– 464, 2004 © 2004 Elsevier Inc. All rights reserved. 360 Park Avenue, South, New York, NY 10010
Serious maternal bradycardia and asystole in laboring parturients after combined spinal-epidural labor analgesia are rare. We report such a case in a morbidly obese laboring parturient after receiving combined spinal-epidural labor analgesia. The differential diagnosis, risk factors, potential contributing factors, and the successful management of the complications with our positive patient outcome are discussed. Even with the low dose of neuraxial drugs commonly administered in combined spinal-epidural labor analgesia, this case underscores the importance of vigilance, frequent monitoring, proper positioning, and rapid resuscitation with escalating doses of ephedrine, atropine, and epinephrine, all of which are essential in the presence of bradycardia or asystole in these patients. © 2004 by Elsevier Inc. Keywords: Analgesia: combined spinal-epidural; anesthesia: obstetrical; asystole; bradycardia; obstetrics.
Introduction In contrast to spinal and epidural anesthesia,1– 8 little to date has been reported on maternal bradycardia or asystole after combined spinal-epidural (CSE) labor analgesia. Here we present such a case in a morbidly obese parturient, which was followed by successful resuscitation and vaginal delivery by forceps. The potential contributing factors and successful management of this serious complication are discussed.
Case Report A 27-year-old, 148-kg, 157-cm, gravida 2 para 0 woman (body mass index of 60 kg/m2), underwent, at 34 weeks’gestation, pitocin augmentation of labor after premature rupture of membrane. After she was administered 1000 mL of lactated Ringer’s solution intravenously (IV), an epidural catheter was placed 0952-8180/04/$–see front matter doi:10.1016/j.jclinane.2003.10.006
Case Reports
successfully at the L3–L4 level on the second attempt. Epidural space was identified by the loss-of-resistance technique at 9 cm; an epidural catheter was inserted 6 cm inside the epidural space and was taped to the skin at the 15-cm mark. After a negative test dose with 3 mL of 2% lidocaine with 1:200,000 epinephrine via the epidural catheter, 5 mL of 1% lidocaine and 5 mL of 0.25% bupivacaine was administered epidurally to obtain a T9– T10 bilateral sensory level blockade, and to achieve patient comfort. An epidural infusion of 0.125% bupivacaine with 2 g/mL of fentanyl was started at a rate of 10 mL/hr. The patient was comfortable and stable until 6 hours later, when she complained of severe labor pain with a 7-cm cervix dilation. At that time, the epidural catheter was found to be dislodged to the 9.5-cm mark on the skin; the patient also had no detectable motor or sensory blockade. After a 500-mL bolus of lactated Ringer’s solution was given, a CSE labor analgesic technique was used. The epidural space was re-identified on the second attempt with loss of resistance obtained 9 cm from skin. Ten g (0.2 mL) sufentanil, 100g (0.1 mL) epinephrine, and 1.75 mg (0.7 mL) bupivacaine were mixed (total: 1 mL) in a syringe and were administered intrathecally after cerebrospinal fluid was identified via a 25-gauge Sprotte needle using a needle-through-needle CSE technique. After removal of the spinal needle, an epidural catheter was inserted with 7 cm inside the epidural space and taped at the 16-cm mark on the skin after negative aspiration test. The patient was comfortable, with a bilateral T8 sensory block and no motor blockade in 5 minutes. Twenty-five minutes later, she complained of rectal pressure at 9 cm cervix dilation. With sensory blockade level still at T9 bilaterally, an epidural test dose (3 mL of 2% lidocaine with 1:200,000 epinephrine) was then administered after repeated negative aspiration. For the first 8 minutes after the epidural test dose, there were no signs of IV or intrathecal injection, or significant changes in motor or sensory functions, vital signs, or mental status. Over the next 2 minutes, the patient stopped talking and then did not respond to verbal commands. On examination, the patient became unresponsive, with a faint pulse of about 30 beats per minutes (bpm), and a shallow respiratory rate (RR) of 12 breaths/min; blood pressure (BP) and pulse oximetry were not obtainable by standard monitors. Resuscitation was initiated immediately with 100% oxygen, assisted mask-ventilation, ephedrine 40 mg IV, bolus infusion of lactated Ringer’s solution, and left tilt position. The patient’s trachea was then intubated and ventilated with 100% oxygen. An electrocardiograph (ECG) was then placed, which revealed asystole, and chest compression was initiated with the patient placed in a laterally tilted position, followed by the simultaneous administration of atropine 1 mg IV. Shortly afterwards, the ECG revealed a sinus tachycardia of 110 bpm with systolic BP (SBP) in the 80 to 90 mmHg range. Pulse oximetry revealed an initial oxygen saturation level of 80% to 85%, which then improved to 96% to 98%. Within 10 minutes, the patient responded with gagging and a periodic intermittent RR of 30 breaths/min and strong movements of all extremities. However, she re462
J. Clin. Anesth., vol. 16, September 2004
mained unresponsive to commands, even after administration of naloxone 0.4 mg IV. At that point, the patient’s hemodynamics were stable. Cervical examination revealed a completely effaced and dilated cervix, and the fetal HR tracing was acceptable, with good variability. The obstetrician requested a vaginal delivery by forceps, with the possibility of a cesarean section. A live infant, with APGAR scores of 8 and 8, was delivered vaginally by forceps. The patient was subsequently transferred to the intensive care unit, and the trachea was extubated 24 hours later without further complications. All laboratory values (CBC, comprehensive metabolic profile, cardiac enzymes profile, coagulation profile) and imaging studies (head magnetic resonance imaging, spiral computed tomography of chest, chest radiography) were within normal limits. The patient was discharged home 2 days later without sequelae.
Discussion The risk factors often cited as associated with cardiac arrest during neuraxial anesthesia are male gender, baseline HR less than 60 bpm, ASA physical status I, use of a beta-blocker, sensory blockade level above T6, age less than 50 years, and a prolonged PR interval.1– 4,9 –12 Despite the increased use of neuraxial labor analgesia, little data has been reported on the occurrence of severe bradycardia or asystole in labor patients.13 Pregnant women may be less likely to develop bradycardia or cardiac arrest during neuraxial anesthesia.11,12,14 Women are 11 to 50 times less likely to develop bradycardia during epidural anesthesia than are men,14 and HR and RR of term parturients are typically higher.11 Furthermore, neuraxial labor analgesia utilizes a dose much lower than those doses used for surgical anesthesia. The differential diagnosis for asystole in this case includes respiratory depression, high or total spinal, local anesthetic toxicity, drug errors, myocardial ischemia, vasovagal reaction, and bradycardic reflexes after neuraxial analgesia. Respiratory depression and mental status changes have been reported to occur within 5 to 20 minutes after intrathecal administration of sufentanil for labor analgesia.5– 8 In these cases of respiratory depression,5– 8 onset was typically more gradual; patients did not develop bradycardia, and with assisted ventilation, oxygenation, and intravenous naloxone, the course reversed quickly. In our patient, the occurrence of bradycardia and asystole occurred about 35 minutes after intrathecal injection of sufentanil and 10 minutes after an epidural test dose, with a change from normal conversation to unresponsiveness occurring within 2 minutes. Furthermore, our patient⬘s respiratory pattern and hemodynamics improved significantly with atropine but not with naloxone. Doses ranging from 3 to 15 g of intrathecal sufentanil alone have been reported to completely relieve labor pain for up to and over 150 minutes, without significant complications.15–20 The intrathecal sufentanil dose we administered was at the higher end of the dose range to maximize the duration of intrathecal analgesia. Furthermore, the anesthetic or analgesic dose required in a morbidly obese patient may be less than for that for a
Asystole after CSE labor analgesia: Pan et al.
non-obese patient. With the efficacy data for labor analgesia from the past few years,15–20 5 g of intrathecal sufentanil together with bupivacaine should already be adequate. Our institutions now use a much smaller dose of intrathecal fentanyl (10 to 15 g) or sufentanil (⬍5 g) with or without bupivacaine for CSE labor analgesia. The morbid obesity of the patient, the hypobaricity of the intrathecal mixture injected, and the epidural volume subsequently injected might have led to a higher than anticipated sympathetic blockade, which can be several dermatomes higher than the sensory blockade.21 Some authors suggested vasodilatation caused by sympathetic blockade during neuraxial anesthesia may be best treated by preemptive fluid administration that is continued after the block is placed.22,23 We administered a 1000-mL bolus of lactated Ringer’s solution IV during the initial placement of the epidural catheter, but we only administered 500 mL during the CSE placement. The volume of IV fluid that we administered might have been inadequate for this patient’s size, especially during the CSE placement, even though the patient did not show any significant hypotension prior to her initial presentation of bradycardia. A high spinal is a possible complication with CSE, especially after a previously failed epidural catheter. Cardiac arrest has been reported by Mackey et al.4 after administration of lidocaine 50 mg for subarachnoid surgical anesthesia. In our patient, the occurrence of bradycardia within 10 minutes of the epidural test dose is certainly suspicious. However, the negative aspiration test, the relatively small dose of lidocaine, the abrupt onset of the events without warning signs, the preserved motor function, and the rapid return to intermittent spontaneous respiration with large tidal volumes, all lead us to exclude a high or total spinal as the etiology. There is a potential risk that previously injected epidural drugs may enter the intrathecal space after a CSE technique. In our case, we chose a CSE technique because of the patient’s rapid labor and lack of residual sensory or motor blockade from previous epidural drugs. To date, ours is the first case report of severe bradycardia or asystole after administration of such a low dose of intrathecal analgesic drugs, and a single epidurally administered epidural test dose in laboring parturients. All previous reports were associated with the larger doses required for surgery. The patient’s bradycardia and asystole are most likely due to a multifactorial combination of morbid obesity, pregnancy, supine hypotension, autonomic disturbances, sympathectomy caused by neuraxial analgesia, and bradycardic reflexes. Morbid obesity alone or together with a gravid uterus in a compromised supine position and sympathectomy after neuraxial analgesia can result in significant aortocaval compression and decrease in venous return. The mechanism of bradycardia is most likely due to one of several mechanisms10,11,24 –26 involving pacemaker stretch, low-pressure baroreceptor in the right atrium and vena cava, or paradoxical Bezold-Jarisch reflex. Our attempt to reposition the patient to a left tilt during resuscitation also played a significant role in the successful resuscitation. Together with a rapid IV fluid bolus, we administered ephedrine 40 mg almost immediately be-
cause we had quick access to it. If atropine and/or epinephrine had been given immediately, they possibly might have reversed the course even more quickly. In conclusion, we report a case of maternal asystole and its successful management in a morbidly obese laboring woman after receiving CSE labor analgesia. Even with the low dose of neuraxial drugs commonly administered for labor analgesia, this case underscores the importance of vigilance, frequent monitoring, proper positioning, and rapid resuscitation with escalating doses of ephedrine, atropine, and epinephrine, which are essential in the presence of bradycardia or asystole in these patients.
References 1. Caplan RA, Ward RJ, Posner K, Cheney FW: Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988;68:5–11. 2. Liguori GA, Sharrock NE: Asystole and severe bradycardia during epidural anesthesia in orthopedic patients. Anesthesiology 1997;86: 250 –7. 3. Lovstad RZ, Granhus G, Hetland S: Bradycardia and asystolic cardiac arrest during spinal anaesthesia: a report of five cases. Acta Anaesthesiol Scand 2000;44:48 –52. 4. Mackey DC, Carpenter RL, Thompson GE, Brown DL, Bodily MN: Bradycardia and asystole during spinal anesthesia: a report of three cases without morbidity. Anesthesiology 1989;70:866 –8. 5. Hays RL, Palmer CM: Respiratory depression after intrathecal sufentanil during labor. Anesthesiology 1994;81:511–2. 6. Greenhalgh CA: Respiratory arrest in a parturient following intrathecal injection of sufentanil and bupivacaine. Anaesthesia 1996;51:173–5. 7. Lu JK, Manullang TR, Staples MH, Kem SE, Balley PL: Maternal respiratory arrests, severe hypotension, and fetal distress after administration of intrathecal, sufentanil, and bupivacaine after intravenous fentanyl. Anesthesiology 1997;87:170 –2. 8. Fragneto RY, Fisher A: Mental status changes and aphasia after labor analgesia with intrathecal sufentanil/bupivacaine. Anesth Analg 2000;90:1175–6. 9. Carpenter RL, Caplan RA, Brown DL, Stephenson C, Wu R: Incidence and risk factors for side effects of spinal anesthesia. Anesthesiology 1992;76:906 –16. 10. Liu S, Paul GE, Carpenter RL, Stephenson C, Wu R: Prolonged PR interval is a risk factor for bradycardia during spinal anesthesia. Reg Anesth 1995;20:41–4. 11. Pollard JB: Common mechanisms and strategies for prevention and treatment of cardiac arrest during epidural anesthesia. J Clin Anesth 2002;14:52–6. 12. Pollard JB: Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesth Analg 2001;92: 252–6. 13. Hawkins JL, Koonin LM, Palmer SK, Gibbs CP: Anesthesiarelated deaths during obstetric delivery in the United States, 1979 –1990. Anesthesiology 1997;86:277–84. 14. Curatolo M, Scaramozzino P, Venuti FS, Orlando A, Zbinden AM: Factors associated with hypotension and bradycardia after epidural blockade. Anesth Analg 1996;83:1033–40. 15. Camann WR, Denney RA, Holby ED, Datta S: A comparison of intrathecal, epidural and intravenous sufentanil for labor analgesia. Anesthesiology 1992;77:884 –7. 16. Honet JE, Arkoosh VA, Norris MC, Huffnagle HJ, Silverman NS, Leighton BL: Comparison among intrathecal fentanyl, meperidine, and sufentanil for labor analgesia. Anesth Analg 1992;75: 734 –9. J. Clin. Anesth., vol. 16, September 2004
463
Case Reports 17. Herman NL, Calicott R, Van Decar TK, Conlin G, Tilton J: Determination of the dose-response relationship for intrathecal sufentanil in laboring patients. Anesth Analg 1997;84:1256 –61. 18. Nelson KE, D’Angelo R, Foss ML, Meister GC, Hood DD, Eisenach JC: Intrathecal neostigmine and sufentanil for early labor analgesia. Anesthesiology 1999;91:1293–8. 19. Arkoosh VA, Cooper M, Norris MC, et al: Intrathecal sufentanil dose response in nulliparous patients. Anesthesiology 1998;89:364 –70. 20. Norris MC, Fogel ST, Holtmann B: Intrathecal sufentanil (5 vs. 10 microg) for labor analgesia: efficacy and side effects. Reg Anesth Pain Med 1998;23:252–7. 21. Choi DH, Park NK, Cho HS, Hahm TS, Chung IS: Effects of epidural injection on spinal block during combined spinal and epidural anesthesia for cesarean delivery. Reg Anesth Pain Med 2000;25:591–5. 22. Mojica JL, Melendez HJ, Bautista LE: The timing of intravenous
464
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23.
24.
25.
26.
crystalloid administration and incidence of cardiovascular side effects during spinal anesthesia: the results from a randomized controlled trial. Anesth Analg 2002;94:432–7. Ewaldsson CA, Hahn RG: Volume kinetics of Ringer’s solution during induction of spinal and general anesthesia. Br J Anaesth 2001;87:406 –14. Goodarzi M, Narasimhan RR: The effect of large-dose intrathecal opioids on the autonomic nervous system. Anesth Analg 2001;93: 456 –9. Kinsella SM, Tuckey JP: Perioperative bradycardia and asystole: relationship to vasovagal syncope and the Bezold-Jarisch reflex. Br J Anaesth 2001;86:859 –68. Baron J, Decaux-Jacolot A, Edouard A, Berdeaux A, Samii K: Influence of venous return on baroreflex control of heart rate during lumbar epidural anesthesia in humans. Anesthesiology 1986;64:188 –93.
*Associate Professor of Anesthesiology, Division of Obstetric Anesthesia, Wake Forest University School of Medicine †Adjunct Professor of Anesthesiology, Division of Obstetric Anesthesia, Medical College of Virginia Health System, Richmond, VA ‡Assistant Professor of Anesthesiology, Division of Obstetric Anesthesia, Wake Forest University School of Medicine Address correspondence to Dr. Pan at the Department of Anesthesiology, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1009, USA. E-mail: [email protected] Presented in part as a poster at the annual meeting for the Society of Obstetric Anesthesia and Perinatology, Hilton Head, SC, May 2002. Received for publication August 6, 2003; revised manuscript accepted for publication October 28, 2003. Journal of Clinical Anesthesia 16:461– 464, 2004 © 2004 Elsevier Inc. All rights reserved. 360 Park Avenue, South, New York, NY 10010
Serious maternal bradycardia and asystole in laboring parturients after combined spinal-epidural labor analgesia are rare. We report such a case in a morbidly obese laboring parturient after receiving combined spinal-epidural labor analgesia. The differential diagnosis, risk factors, potential contributing factors, and the successful management of the complications with our positive patient outcome are discussed. Even with the low dose of neuraxial drugs commonly administered in combined spinal-epidural labor analgesia, this case underscores the importance of vigilance, frequent monitoring, proper positioning, and rapid resuscitation with escalating doses of ephedrine, atropine, and epinephrine, all of which are essential in the presence of bradycardia or asystole in these patients. © 2004 by Elsevier Inc. Keywords: Analgesia: combined spinal-epidural; anesthesia: obstetrical; asystole; bradycardia; obstetrics.
Introduction In contrast to spinal and epidural anesthesia,1– 8 little to date has been reported on maternal bradycardia or asystole after combined spinal-epidural (CSE) labor analgesia. Here we present such a case in a morbidly obese parturient, which was followed by successful resuscitation and vaginal delivery by forceps. The potential contributing factors and successful management of this serious complication are discussed.
Case Report A 27-year-old, 148-kg, 157-cm, gravida 2 para 0 woman (body mass index of 60 kg/m2), underwent, at 34 weeks’gestation, pitocin augmentation of labor after premature rupture of membrane. After she was administered 1000 mL of lactated Ringer’s solution intravenously (IV), an epidural catheter was placed 0952-8180/04/$–see front matter doi:10.1016/j.jclinane.2003.10.006
Case Reports
successfully at the L3–L4 level on the second attempt. Epidural space was identified by the loss-of-resistance technique at 9 cm; an epidural catheter was inserted 6 cm inside the epidural space and was taped to the skin at the 15-cm mark. After a negative test dose with 3 mL of 2% lidocaine with 1:200,000 epinephrine via the epidural catheter, 5 mL of 1% lidocaine and 5 mL of 0.25% bupivacaine was administered epidurally to obtain a T9– T10 bilateral sensory level blockade, and to achieve patient comfort. An epidural infusion of 0.125% bupivacaine with 2 g/mL of fentanyl was started at a rate of 10 mL/hr. The patient was comfortable and stable until 6 hours later, when she complained of severe labor pain with a 7-cm cervix dilation. At that time, the epidural catheter was found to be dislodged to the 9.5-cm mark on the skin; the patient also had no detectable motor or sensory blockade. After a 500-mL bolus of lactated Ringer’s solution was given, a CSE labor analgesic technique was used. The epidural space was re-identified on the second attempt with loss of resistance obtained 9 cm from skin. Ten g (0.2 mL) sufentanil, 100g (0.1 mL) epinephrine, and 1.75 mg (0.7 mL) bupivacaine were mixed (total: 1 mL) in a syringe and were administered intrathecally after cerebrospinal fluid was identified via a 25-gauge Sprotte needle using a needle-through-needle CSE technique. After removal of the spinal needle, an epidural catheter was inserted with 7 cm inside the epidural space and taped at the 16-cm mark on the skin after negative aspiration test. The patient was comfortable, with a bilateral T8 sensory block and no motor blockade in 5 minutes. Twenty-five minutes later, she complained of rectal pressure at 9 cm cervix dilation. With sensory blockade level still at T9 bilaterally, an epidural test dose (3 mL of 2% lidocaine with 1:200,000 epinephrine) was then administered after repeated negative aspiration. For the first 8 minutes after the epidural test dose, there were no signs of IV or intrathecal injection, or significant changes in motor or sensory functions, vital signs, or mental status. Over the next 2 minutes, the patient stopped talking and then did not respond to verbal commands. On examination, the patient became unresponsive, with a faint pulse of about 30 beats per minutes (bpm), and a shallow respiratory rate (RR) of 12 breaths/min; blood pressure (BP) and pulse oximetry were not obtainable by standard monitors. Resuscitation was initiated immediately with 100% oxygen, assisted mask-ventilation, ephedrine 40 mg IV, bolus infusion of lactated Ringer’s solution, and left tilt position. The patient’s trachea was then intubated and ventilated with 100% oxygen. An electrocardiograph (ECG) was then placed, which revealed asystole, and chest compression was initiated with the patient placed in a laterally tilted position, followed by the simultaneous administration of atropine 1 mg IV. Shortly afterwards, the ECG revealed a sinus tachycardia of 110 bpm with systolic BP (SBP) in the 80 to 90 mmHg range. Pulse oximetry revealed an initial oxygen saturation level of 80% to 85%, which then improved to 96% to 98%. Within 10 minutes, the patient responded with gagging and a periodic intermittent RR of 30 breaths/min and strong movements of all extremities. However, she re462
J. Clin. Anesth., vol. 16, September 2004
mained unresponsive to commands, even after administration of naloxone 0.4 mg IV. At that point, the patient’s hemodynamics were stable. Cervical examination revealed a completely effaced and dilated cervix, and the fetal HR tracing was acceptable, with good variability. The obstetrician requested a vaginal delivery by forceps, with the possibility of a cesarean section. A live infant, with APGAR scores of 8 and 8, was delivered vaginally by forceps. The patient was subsequently transferred to the intensive care unit, and the trachea was extubated 24 hours later without further complications. All laboratory values (CBC, comprehensive metabolic profile, cardiac enzymes profile, coagulation profile) and imaging studies (head magnetic resonance imaging, spiral computed tomography of chest, chest radiography) were within normal limits. The patient was discharged home 2 days later without sequelae.
Discussion The risk factors often cited as associated with cardiac arrest during neuraxial anesthesia are male gender, baseline HR less than 60 bpm, ASA physical status I, use of a beta-blocker, sensory blockade level above T6, age less than 50 years, and a prolonged PR interval.1– 4,9 –12 Despite the increased use of neuraxial labor analgesia, little data has been reported on the occurrence of severe bradycardia or asystole in labor patients.13 Pregnant women may be less likely to develop bradycardia or cardiac arrest during neuraxial anesthesia.11,12,14 Women are 11 to 50 times less likely to develop bradycardia during epidural anesthesia than are men,14 and HR and RR of term parturients are typically higher.11 Furthermore, neuraxial labor analgesia utilizes a dose much lower than those doses used for surgical anesthesia. The differential diagnosis for asystole in this case includes respiratory depression, high or total spinal, local anesthetic toxicity, drug errors, myocardial ischemia, vasovagal reaction, and bradycardic reflexes after neuraxial analgesia. Respiratory depression and mental status changes have been reported to occur within 5 to 20 minutes after intrathecal administration of sufentanil for labor analgesia.5– 8 In these cases of respiratory depression,5– 8 onset was typically more gradual; patients did not develop bradycardia, and with assisted ventilation, oxygenation, and intravenous naloxone, the course reversed quickly. In our patient, the occurrence of bradycardia and asystole occurred about 35 minutes after intrathecal injection of sufentanil and 10 minutes after an epidural test dose, with a change from normal conversation to unresponsiveness occurring within 2 minutes. Furthermore, our patient⬘s respiratory pattern and hemodynamics improved significantly with atropine but not with naloxone. Doses ranging from 3 to 15 g of intrathecal sufentanil alone have been reported to completely relieve labor pain for up to and over 150 minutes, without significant complications.15–20 The intrathecal sufentanil dose we administered was at the higher end of the dose range to maximize the duration of intrathecal analgesia. Furthermore, the anesthetic or analgesic dose required in a morbidly obese patient may be less than for that for a
Asystole after CSE labor analgesia: Pan et al.
non-obese patient. With the efficacy data for labor analgesia from the past few years,15–20 5 g of intrathecal sufentanil together with bupivacaine should already be adequate. Our institutions now use a much smaller dose of intrathecal fentanyl (10 to 15 g) or sufentanil (⬍5 g) with or without bupivacaine for CSE labor analgesia. The morbid obesity of the patient, the hypobaricity of the intrathecal mixture injected, and the epidural volume subsequently injected might have led to a higher than anticipated sympathetic blockade, which can be several dermatomes higher than the sensory blockade.21 Some authors suggested vasodilatation caused by sympathetic blockade during neuraxial anesthesia may be best treated by preemptive fluid administration that is continued after the block is placed.22,23 We administered a 1000-mL bolus of lactated Ringer’s solution IV during the initial placement of the epidural catheter, but we only administered 500 mL during the CSE placement. The volume of IV fluid that we administered might have been inadequate for this patient’s size, especially during the CSE placement, even though the patient did not show any significant hypotension prior to her initial presentation of bradycardia. A high spinal is a possible complication with CSE, especially after a previously failed epidural catheter. Cardiac arrest has been reported by Mackey et al.4 after administration of lidocaine 50 mg for subarachnoid surgical anesthesia. In our patient, the occurrence of bradycardia within 10 minutes of the epidural test dose is certainly suspicious. However, the negative aspiration test, the relatively small dose of lidocaine, the abrupt onset of the events without warning signs, the preserved motor function, and the rapid return to intermittent spontaneous respiration with large tidal volumes, all lead us to exclude a high or total spinal as the etiology. There is a potential risk that previously injected epidural drugs may enter the intrathecal space after a CSE technique. In our case, we chose a CSE technique because of the patient’s rapid labor and lack of residual sensory or motor blockade from previous epidural drugs. To date, ours is the first case report of severe bradycardia or asystole after administration of such a low dose of intrathecal analgesic drugs, and a single epidurally administered epidural test dose in laboring parturients. All previous reports were associated with the larger doses required for surgery. The patient’s bradycardia and asystole are most likely due to a multifactorial combination of morbid obesity, pregnancy, supine hypotension, autonomic disturbances, sympathectomy caused by neuraxial analgesia, and bradycardic reflexes. Morbid obesity alone or together with a gravid uterus in a compromised supine position and sympathectomy after neuraxial analgesia can result in significant aortocaval compression and decrease in venous return. The mechanism of bradycardia is most likely due to one of several mechanisms10,11,24 –26 involving pacemaker stretch, low-pressure baroreceptor in the right atrium and vena cava, or paradoxical Bezold-Jarisch reflex. Our attempt to reposition the patient to a left tilt during resuscitation also played a significant role in the successful resuscitation. Together with a rapid IV fluid bolus, we administered ephedrine 40 mg almost immediately be-
cause we had quick access to it. If atropine and/or epinephrine had been given immediately, they possibly might have reversed the course even more quickly. In conclusion, we report a case of maternal asystole and its successful management in a morbidly obese laboring woman after receiving CSE labor analgesia. Even with the low dose of neuraxial drugs commonly administered for labor analgesia, this case underscores the importance of vigilance, frequent monitoring, proper positioning, and rapid resuscitation with escalating doses of ephedrine, atropine, and epinephrine, which are essential in the presence of bradycardia or asystole in these patients.
References 1. Caplan RA, Ward RJ, Posner K, Cheney FW: Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988;68:5–11. 2. Liguori GA, Sharrock NE: Asystole and severe bradycardia during epidural anesthesia in orthopedic patients. Anesthesiology 1997;86: 250 –7. 3. Lovstad RZ, Granhus G, Hetland S: Bradycardia and asystolic cardiac arrest during spinal anaesthesia: a report of five cases. Acta Anaesthesiol Scand 2000;44:48 –52. 4. Mackey DC, Carpenter RL, Thompson GE, Brown DL, Bodily MN: Bradycardia and asystole during spinal anesthesia: a report of three cases without morbidity. Anesthesiology 1989;70:866 –8. 5. Hays RL, Palmer CM: Respiratory depression after intrathecal sufentanil during labor. Anesthesiology 1994;81:511–2. 6. Greenhalgh CA: Respiratory arrest in a parturient following intrathecal injection of sufentanil and bupivacaine. Anaesthesia 1996;51:173–5. 7. Lu JK, Manullang TR, Staples MH, Kem SE, Balley PL: Maternal respiratory arrests, severe hypotension, and fetal distress after administration of intrathecal, sufentanil, and bupivacaine after intravenous fentanyl. Anesthesiology 1997;87:170 –2. 8. Fragneto RY, Fisher A: Mental status changes and aphasia after labor analgesia with intrathecal sufentanil/bupivacaine. Anesth Analg 2000;90:1175–6. 9. Carpenter RL, Caplan RA, Brown DL, Stephenson C, Wu R: Incidence and risk factors for side effects of spinal anesthesia. Anesthesiology 1992;76:906 –16. 10. Liu S, Paul GE, Carpenter RL, Stephenson C, Wu R: Prolonged PR interval is a risk factor for bradycardia during spinal anesthesia. Reg Anesth 1995;20:41–4. 11. Pollard JB: Common mechanisms and strategies for prevention and treatment of cardiac arrest during epidural anesthesia. J Clin Anesth 2002;14:52–6. 12. Pollard JB: Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesth Analg 2001;92: 252–6. 13. Hawkins JL, Koonin LM, Palmer SK, Gibbs CP: Anesthesiarelated deaths during obstetric delivery in the United States, 1979 –1990. Anesthesiology 1997;86:277–84. 14. Curatolo M, Scaramozzino P, Venuti FS, Orlando A, Zbinden AM: Factors associated with hypotension and bradycardia after epidural blockade. Anesth Analg 1996;83:1033–40. 15. Camann WR, Denney RA, Holby ED, Datta S: A comparison of intrathecal, epidural and intravenous sufentanil for labor analgesia. Anesthesiology 1992;77:884 –7. 16. Honet JE, Arkoosh VA, Norris MC, Huffnagle HJ, Silverman NS, Leighton BL: Comparison among intrathecal fentanyl, meperidine, and sufentanil for labor analgesia. Anesth Analg 1992;75: 734 –9. J. Clin. Anesth., vol. 16, September 2004
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