Neuraxial anesthesia and External Cephalic Version

ACOG: If Your Baby is Breech

What is an external cephalic version?

External-Cephalic-Version
From Pregmed.org

Wikipedia: external cephalic version


Randomized trial of anaesthetic interventions in external cephalic version for breech presentation. British Journal of Anaesthesia 114 (6): 944–50 (2015)

  • Conclusions: Spinal Anesthesia (SA: hyperbaric bupivacaine 9mg + fentanyl 15mcg) increased the success rate and reduced pain for both primary and re-attempts of External Cephalic Version (ECV), whereas IV Anesthesia (IVA) using remifentanil infusion (0.1mcg/kg/min) only reduced the pain. There was no significant increase in the incidence of fetal bradycardia or emergency CS, with ECV performed under anaesthetic interventions. Relaxation of the abdominal muscles from SA appears to underlie the improved outcomes for ECV.
  • Editor’s key points: There is no consensus on best anaesthetic technique for external cephalic version (ECV).  In this study, success at ECV was higher using spinal anaesthesia compared with remifentanil infusion or no intervention.  Pain was also reduced in the remifentanil group but success at ECV was no different to the no intervention group.  The effect of spinal anaesthesia in ECV may relate to relaxation of the abdominal musculature.

Neuraxial blockade for external cephalic version: Cost analysis. J Obstet Gynaecol Res. 2015 Jul; 41(7): 1023–1031.

  • Neuraxial blockade is associated with minimal hospital and insurer cost changes in the setting of external cephalic version, while reducing the cesarean delivery rate.

External cephalic version with or without spinal anesthesia: a cost-effectiveness analysis.  American Journal of Obstetrics and Gynecology, January 2016Volume 214, Issue 1, Supplement, Pages S206–S207.  

  • It is both effective and cost-effective to utilize spinal anesthesia to perform ECV in term, nulliparous women with breech fetuses. Translation of this potentially impactful approach into broad obstetric practice should be undertaken.

Effect of Regional Anesthesia on the Success Rate of External Cephalic Version: A Systematic Review and Meta-Analysis. Obstet Gynecol. 2011 Nov; 118(5): 1137–1144.

  • Six RCTs met criteria for study inclusion. Regional anesthesia was associated with a higher external cephalic version success rate compared to intravenous or no analgesia (59.7% vs. 37.6%; pooled RR 1.58, 95% confidence interval [CI] 1.29-1.93). This significant association persisted when the data was stratified by type of regional anesthesia (spinal vs. epidural). The number needed to treat with regional anesthesia to achieve one additional successful ECV was 5. There was no evidence of statistical heterogeneity (p=0.32, I2=14.9%) or publication bias (Harbord test p=0.78). There was no statistically significant difference in the risk of cesarean delivery comparing regional anesthesia to intravenous or no analgesia (48.4% vs. 59.3%; pooled RR 0.80, 95% CI 0.55-1.17). Adverse events were rare and not significantly different between the two groups.

Does Regional Anesthesia for External Cephalic Version Increase the Risk of Emergent Cesarean Delivery? Obstetrics & Gynecology: May 2016

  • Neuraxial Anesthesia (NA) for External Cephalic Version (ECV) increased the risk of emergent cesarean delivery (CD) without impacting ECV success. These findings differ from previous randomized controlled trials (RCTs). The increased risk and decreased success of our ECVs compared to ECVs performed in the context of RCTs could be explained by patient selection, variation in operator experience or technique, or variation in anesthetic management.  Future studies should further evaluate the risk of NA for ECV in true practice scenarios outside of RCTs.

Clinical outcomes after external cephalic version with spinal anesthesia after failure of a first attempt without anesthesia.  International Journal of Obstetrics & Gynecology. Volume139, Issue3. December 2017: 324-328.

  • Repeat ECV with spinal anesthesia after a failed first attempt without spinal anesthesia increased vertex presentation at birth and decreased the rate of cesarean delivery.

Effect of Intrathecal Bupivacaine Dose on the Success of External Cephalic Version for Breech Presentation: A Prospective, Randomized, Blinded Clinical Trial. Anesthesiology 10 2017, Vol.127, 625-632.

  • Results: A total of 240 subjects were enrolled, and 239 received the intervention. External cephalic version was successful in 123 (51.5%) of 239 patients. Compared with bupivacaine 2.5 mg, the odds (99% CI) for a successful version were 1.0 (0.4 to 2.6), 1.0 (0.4 to 2.7), and 0.9 (0.4 to 2.4) for bupivacaine 5.0, 7.5, and 10.0 mg, respectively (P = 0.99). There were no differences in the cesarean delivery rate (P = 0.76) or indication for cesarean delivery (P = 0.82). Time to discharge was increased 60 min (16 to 116 min) with bupivacaine 7.5 mg or higher as compared with 2.5 mg (P = 0.004).
  • Conclusions: A dose of intrathecal bupivacaine greater than 2.5 mg does not lead to an additional increase in external cephalic procedural success or a reduction in cesarean delivery.

 

 

 

 

Methadone and Acute and Chronic Pain Management

We had a journal club where we discussed this article: Anesthesiology, May 2017; Clinical effectiveness and safety of intraoperative methadone in patients undergoing posterior spinal fusion surgery: a randomized, double-blinded, controlled trial.

  • IV Methadone 0.2 mg/kg vs IV hydromorphone 2mg at surgical closure in 2+ level spinal fusion
  • Decreased postop IV and opioid requirements and pain scores.  Improved patient satisfaction

Questions:

  1. Is there a pain service following these patients postoperatively?
  2. Exclusions: do you include OSA and BMI>45 patients?
  3. Is ETCO2 and PCA enough to combat respiratory depression on the floor?
  4. Are any discharged on the same day after receiving this dose — think total knees and single level lamis?
  5. Will this improve or worsen the opioid epidemic?
  6. Are surgeons on board with tackling pain multimodally for the benefit of the patient?
  7. For pain follow-up, are there psychiatry, homeopathy, palliative care, PT, holistic approaches for the patient?

Methadone Dose Conversion Guidelines

Intraop Lidocaine for postop pain

Intraop Ketamine for postop pain

Literature search:

Sys Rev 2014: Effectiveness of opioid substitution treatments for patients with opioid dependence: a systematic review and multiple treatment protocol.

Am j of Pub Health, Aug 2014. Determinants of Increased Opioid-Related Mortality in the United States and Canada, 1990–2013: A Systematic Review.

Br J Clin Pharmacol. 2014 Feb; 77(2): 272–284. Long term outcomes of pharmacological treatments for opioid dependence: does methadone still lead the pack?

PLoS One. 2014; 9(11): e112328. Methadone Induction in Primary Care for Opioid Dependence: A Pragmatic Randomized Trial (ANRS Methaville).

Curr Psychiatry Rev. 2014 May; 10(2): 156–167. Genetics of Opioid Dependence: A Review of the Genetic Contribution to Opioid Dependence. 

Drug Alcohol Depend. 2016 Mar 1; 160: 112–118. Methadone, Buprenorphine and Preferences for Opioid Agonist Treatment: A Qualitative Analysis. 

Croat Med J. 2013 Feb; 54(1): 42–48. Risk factors for fatal outcome in patients with opioid dependence treated with methadone in a family medicine setting in Croatia. 

J Med Toxicol. 2016 Mar; 12(1): 58–63. Pharmacotherapy of Opioid Addiction: “Putting a Real Face on a False Demon”. 

Syst Rev. 2014; 3: 45. Sex differences in outcomes of methadone maintenance treatment for opioid addiction: a systematic review protocol.

Your brain under anesthesia

Anesthesiology 10 2015, Vol.123, 937-960. Clinical Electroencephalography for Anesthesiologists: Part I: Background and Basic Signatures
Patrick L. Purdon, Ph.D.; Aaron Sampson, B.S.; Kara J. Pavone, B.S.; Emery N. Brown, M.D., Ph.D.

Unprocessed electroencephalogram signatures of propofol-induced sedation and unconsciousness. (A) Awake eyes open electroencephalogram pattern. (B) Paradoxical excitation. (C) Alpha and beta oscillations commonly observed during propofol-induced sedation (fig. 5). (D) Slow-delta and alpha oscillations commonly seen during unconsciousness. (E) Slow oscillations commonly observed during unconsciousness at induction with propofol (fig. 6) and sedation with dexmedetomidine (fig. 11) and with nitrous oxide (fig. 13). (F) Burst suppression, a state of profound anesthetic-induced brain inactivation commonly occurring in elderly patients,68 anesthetic-induced coma, and profound hypothermia (fig. 6, B and D). (G) Isoelectric electroencephalogram pattern commonly observed in anesthetic-induced coma and profound hypothermia. With the exception of the isoelectric state, the amplitudes of the electroencephalogram signatures of the anesthetized states are larger than the amplitudes of the electroencephalogram in the awake state by a factor of 5 to 20. All electroencephalogram recordings are from the same subject. Reproduced, with permission, from Brown et al. Chapter 50 in Miller’s Anesthesia, 8th edition, 2014.

The brain on propofol.  

A is adapted, with permission, from Purdon et al:Electroencephalogram signatures of loss and recovery of consciousness from propofol. Proc Natl Acad Sci U S A 2013; 110:E1142–51; and C is adapted, with permission, from Lewis et al. Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness. Proc Natl Acad Sci U S A2012; 109:E3377–86. Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.


(A) At low doses, ketamine blocks preferentially the actions of glutamate N-methyl-d-aspartate receptors on γ-aminobutyric acid (GABA)ergic inhibitory interneurons in the cortex and subcortical sites such as the thalamus, hippocampus, and the limbic system. The antinociceptive effect of ketamine is due in part to its blockade of glutamate release from peripheral afferent (PAF) neurons in the dorsal root ganglia (DRG) at their synapses on to projection neurons (PNs) in the spinal cord. (B) Spectrogram showing the beta-gamma oscillations in the electroencephalogram of a 61-yr-old woman who received ketamine administered in 30 mg and 20 mg doses (green arrows) for a vacuum dressing change. Blocking the inhibitory action of the interneurons in cortical and subcortical circuits helps explain why ketamine produces beta oscillations as its electroencephalogram signature. (C) Ten-second electroencephalogram trace recorded at minute 5 from the spectrogram in B. A is reproduced, with permission, from Brown, Purdon, and Van Dort: General anesthesia and altered states of arousal: A systems neuroscience analysis. Annu Rev Neurosci. 2011;324:601–28. B and C were adapted from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), with permission, from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.


Spectrograms and time domain electroencephalogram signatures of dexmedetomidine-induced sedation. (A) Spectrogram of the electroencephalogram of a 59-kg patient receiving a 0.65 μg kg−1 h−1 dexmedetomidine infusion to maintain sedation. The spectrogram shows spindles (9 to 15 Hz oscillations) and slow-delta oscillations. (B) Ten-second electroencephalogram trace recorded at minute 60 from the spectrogram in A emphasizing spindles (red underlines). (C) Spectrogram of the electroencephalogram of a 65-kg patient receiving a 0.85 μg kg−1 h−1 dexmedetomidine infusion to maintain sedation. (D) Ten-second electroencephalogram trace recorded at minute 40 from the spectrogram in C showing the slow-delta oscillations. A–D were adapted, with permission, from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.

Spectrograms and time domain electroencephalogram signatures of sevoflurane, isoflurane, and desflurane at surgical levels of unconsciousness. The inspired concentration of the anesthetics is the blue trace in the upper part of each panel. Green arrows below each panel are propofol bolus doses. (A) At sub-minimal alveolar concentrations (MACs) (minutes 40 to 60), the spectrogram of sevoflurane resembles that of propofol (fig. 6, A and B). As the concentration of sevoflurane is increased (minutes 100 to 120), theta (5 to 7Hz) oscillations appear. The theta oscillations dissipate when the sevoflurane concentration (blue curve) is decreased. (B) Ten-second electroencephalogram trace of sevoflurane recorded at minute 40 of the spectrogram in A. (C) The spectrogram of sevoflurane shows constant alpha, slow, delta and theta oscillations at a constant concentration of 3%. (D) Ten-second electroencephalogram trace of sevoflurane recorded at minute 30 of the spectrogram in C. (E) At sub-MAC concentrations (minutes 16 to 26), the spectrogram of isoflurane resembles that of propofol (fig. 6, A and B) and sub-MAC sevoflurane (A). Theta oscillations strengthen as the isoflurane concentration increases toward MAC. (F) Ten-second electroencephalogram trace of isoflurane recorded at minute 40 of the spectrogram in E. (G) At the sub-MAC concentrations shown here, the spectrogram of desflurane resembles propofol with very low theta oscillation power. (H) Ten-second electroencephalogram trace of isoflurane recorded at minute 40 of the spectrogram in G. A, C, E, and G were adapted, with permission, from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.

Slow-delta and beta-gamma oscillations associated with nitrous oxide. (A) Prior to emergence, a patient was maintained on 0.5% isoflurane and 58% oxygen. At minute 82, the composition of the anesthetic gases was changed to 0.2% isoflurane (blue curve) in 75% nitrous oxide (green curve) and 24% oxygen. The total gas flow was increased from 3 to 7 l/min. The alpha, theta, and slow oscillation power decreased from minutes 83 to 85. At minute 86, the power in the theta to beta bands decreased considerably (blue area) as the slow-delta oscillation power increased. At minute 89, the slow-delta oscillation power decreased and the beta-gamma oscillations appeared at minute 90. The flow rates and anesthetic concentrations were maintained constant between minutes 82 and 91. Isoflurane was turned off at minute 91. (B) Ten-second electroencephalogram traces of the slow-delta oscillation at minute 86.7 and the beta-gamma oscillations at minute 90.8. A and B were adapted, with permission, from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.

Different anesthetics (propofol, sevoflurane, ketamine, and dexmedetomidine), different electroencephalogram signatures, and different molecular and neural circuit mechanisms. (A) Anesthetic-specific differences in the electroencephalogram are difficult to discern in unprocessed electroencephalogram waveforms. (B) In the spectrogram, it is clear that different anesthetics produce different electroencephalogram signatures. The dynamics the electroencephalogram signatures can be related to the molecular targets and the neural circuits at which the anesthetics act to create altered states of arousal. Propofol and sevoflurane enhance γ-aminobutyric acid (GABA)ergic inhibition, sevoflurane binds at GABA receptors and other molecular targets, ketamine blocks N-methyl-d-aspartate (NMDA) glutamate receptors, and dexmedetomidine is a presynaptic alpha adrenergic agonist. A and B were adapted, with permission, from Purdon and Brown, Clinical Electroencephalography for the Anesthesiologist (2014), from the Partners Healthcare Office of Continuing Professional Development.69 Adaptations are themselves works protected by copyright. In order to publish this adaptation, authorization has been obtained both from the owner of the copyright of the original work and from the owner of copyright of the translation or adaptation.

Key points:

  • For the inhaled ether-derived anesthetics such as sevoflurane, isoflurane, and desflurane, we observed that, with the exception of the theta oscillations that appear around 1 MAC and beyond, their electroencephalogram patterns during maintenance and emergence closely resemble those seen in propofol. Nitrous oxide is known to be associated with increased beta and gamma oscillations and likely decreased slow-delta oscillations. However, we demonstrated that nitrous oxide also produces profound slow-delta oscillations during the transition from an inhaled ether anesthetic.
  • An animated version of portions of parts I and II are available at www.AnesthesiaEEG.com.