CORRESPONDENCE
Response to the letter of Dr. B Haydar SIR—In response to the letter of Dr. Bishr Haydar. We thank Dr. Haydar for his interest in and comments about our case report of an unintentional epidural injection of epinephrine (1,2). We agree with the concern that knowledge is building regarding the function of the ICON monitor, but do not see why ‘the picture may become muddied’ simply by having some information that would not otherwise be available. The issue that we reported was surprising in that the onset of epinephrine absorbed via the caudal space was gradual and not rapid as one would see with intravenous administration. What was also of great interest was that changes in standard hemodynamic parameters such as heart rate and systolic blood pressure were not as pronounced as might have been anticipated. The accuracy of the ICON may decrease in the face of extreme tachycardia or pulmonary edema, but our patient exhibited neither of these signs. We understand Dr. Haydar’s opinion that our results should be viewed ‘cautiously’, but suggest that caution should follow only from the inherent one-time nature of any case report, not from deficiencies in the ICON’s ability to accurately monitor this event. We agree that a higher concentration of epinephrine being administered would have been of greater concern. Indeed, one author (CJC) has seen a vial swap in which a child who received 1 mg of epinephrine developed severe hypertension, tachycardia, and pulmonary edema. In our case, however, an analogous situation would have required someone to draw up three separate 1 mg epinephrine vials into a single syringe—an implausible event under virtually any circumstances. Regarding the issue of root cause analysis, we were a bit stunned with the suggestion that a research device or the presence of researchers distracted the anesthesia team. Our study was designed simply around a research fellow placing four EKG electrodes before anesthesia induction followed by passive data collection and offline analysis. No action by the anesthesia team (even including looking at the ICON monitor) was required. The research fellow stood in the background and had no further conversations with the anesthesiologists unless an event occurred, in which case the team was queried for details only after the clinical issue had been resolved. Dr. Haydar makes a generically valid point that clinical research may possibly lead to inattentiveness. However,
© 2015 John Wiley & Sons Ltd Pediatric Anesthesia 25 (2015) 753–760
in our case, distraction from the research protocol could not, and did not, occur. There was no ‘reverse Hawthorne’ effect. Our initial submission did include a root cause analysis and discussion of how to reduce syringe swaps, but the editors asked us to omit this material as the topic is well described in the literature. In short, multiple issues contributed to this particular event: a last-minute change in anesthesiologists; production pressure; equipment set up and medication preparation by multiple individuals; variability in syringe labeling and anesthesia workspace configuration practices among practitioners; bupivacaine not yet programmed into the library of a new label-maker machine; and a visual washout effect of certain drug-label colors against a blue towel. While most of these events are prosaic in current anesthesia practice, in this case they aligned so as to create a unique ‘Swiss cheese’ medical error. As to Dr. Haydar’s question of what systemic changes were actually implemented at our institution after this event, the answer is that a two-person drug readback now occurs before pediatric caudal blockade—a double-check that has also been discussed in the context of other adverse drug events (3). Finally, the reason for the publication delay was to ensure no harm to the child after adequate follow-up. This was perhaps the most valuable part of the report. Ethics approval None required for this manuscript. Funding The study received no external funding. Conflict of interest The authors report no conflict of interest. David A. August & Charles J. Cote Division of Pediatric Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA Email: [email protected] doi:10.1111/pan.12661
753
Correspondence
References 1 August DA, Sui J, Cote CJ. Unintentional epidural injection of 88 lgkg 1 of epinephrine. Pediatr Anesth 2014; 24: 1185–1187.
2 Haydar B. Harm attributable to research distraction? Challenging conclusions on caudal epinephrine. Pediatr Anesth 2014; 24: 1313–1314.
3 O’Connor M. Responsiveness to the chlorhexidine epidural tragedy: a mental block? J Law Med 2012; 19: 436–443.
Craniosynostosis reconstruction in patients with cyanotic heart defects—risk factors for venous air embolism and overview of preventative strategies SIR—We commend the authors, Bergmans et al. (1), for a thoughtful case report of craniosynostosis surgery in an infant with complex congenital heart disease. The judicious replacement of intraoperative blood loss and use of a higher transfusion threshold owing to the patient’s chronic hypoxia and tendency toward polycythemia were indispensable to the success of the operation. While the report addresses crucial issues of perioperative monitoring and hemodynamic management, we would also like to bring attention to a unique perioperative risk in this patient population—the risk of venous air embolism (VAE). Reports of the incidence of VAE during craniosynostosis repair ranges from 8 to 82.6% (2,3). Recognition of VAE is of particular importance in patients with cardiac defects and right-to-left shunts due to the high risk of developing paradoxical arterial emboli. A small amount of air into the cerebral or coronary circulation can be fatal. The patient described had a double outlet right ventricle, multiple ventricular septal defects, atrial septal defect, and transposition of the great vessels. This anatomy placed the patient at risk for arterial emboli due to mixing within the dominant right ventricle and a smaller fraction of pulmonary arterial flow, thereby diminishing the capacity of pulmonary vessels to potentially filter air emboli. In addition, patient positioning during craniofacial and neurosurgical procedures increases the inherent risk of VAE by virtue of the surgical site being elevated above the level of the right atrium. Monitoring for VAE is important and signs of VAE include sudden drop in blood pressure, characteristic change in Doppler tones, decreased endtidal carbon dioxide (ETCO2), increased central venous pressure (CVP), decreased oxygen saturation, right ventricular strain pattern on the EKG, and increased pulmonary artery pressure. In the event that a VAE is suspected, the following measures should be taken (3–5): prompt flooding of the surgical
754
field with saline, continuous monitoring of end-tidal carbon dioxide (ETCO2) and nitrogen (if possible), use of bone wax to prevent entry of atmospheric air, use of precordial Doppler ultrasonography for detection, search for open venous sinuses, and strict intra-arterial blood pressure monitoring. Additional therapeutic maneuvers include aspiration via right atrial catheter and left lateral decubitus or Trendelenburg positioning. Interestingly, this patient’s unique physiology may have potentially reduced the risk of VAE in one respect—the confluence of cardiac defects resulted in an elevated CVP (9–14 mmHg). As jugular venous pressure was already above atmospheric pressure, violation of a vein would favor bleeding instead of air entrainment. Management of patients with comorbid congenital anomalies necessitates the collaboration of multiple disciplines. This approach allows risk reduction with appreciation of each patient’s relevant anatomic and physiologic aberrancies. The occurrence of VAE is exceptionally ominous in patients with cardiac defects, thus intraoperative avoidance, detection, and response are paramount to maximizing patient safety. Communication among all treating specialists is critical both during the time-out process and during the surgical procedure to optimize patient outcomes. Acknowledgments None. Funding The study received no external funding. Conflict of interest The authors report no conflict of interest.
© 2015 John Wiley & Sons Ltd Pediatric Anesthesia 25 (2015) 753–760
Response to the letter of Dr. B Haydar SIR—In response to the letter of Dr. Bishr Haydar. We thank Dr. Haydar for his interest in and comments about our case report of an unintentional epidural injection of epinephrine (1,2). We agree with the concern that knowledge is building regarding the function of the ICON monitor, but do not see why ‘the picture may become muddied’ simply by having some information that would not otherwise be available. The issue that we reported was surprising in that the onset of epinephrine absorbed via the caudal space was gradual and not rapid as one would see with intravenous administration. What was also of great interest was that changes in standard hemodynamic parameters such as heart rate and systolic blood pressure were not as pronounced as might have been anticipated. The accuracy of the ICON may decrease in the face of extreme tachycardia or pulmonary edema, but our patient exhibited neither of these signs. We understand Dr. Haydar’s opinion that our results should be viewed ‘cautiously’, but suggest that caution should follow only from the inherent one-time nature of any case report, not from deficiencies in the ICON’s ability to accurately monitor this event. We agree that a higher concentration of epinephrine being administered would have been of greater concern. Indeed, one author (CJC) has seen a vial swap in which a child who received 1 mg of epinephrine developed severe hypertension, tachycardia, and pulmonary edema. In our case, however, an analogous situation would have required someone to draw up three separate 1 mg epinephrine vials into a single syringe—an implausible event under virtually any circumstances. Regarding the issue of root cause analysis, we were a bit stunned with the suggestion that a research device or the presence of researchers distracted the anesthesia team. Our study was designed simply around a research fellow placing four EKG electrodes before anesthesia induction followed by passive data collection and offline analysis. No action by the anesthesia team (even including looking at the ICON monitor) was required. The research fellow stood in the background and had no further conversations with the anesthesiologists unless an event occurred, in which case the team was queried for details only after the clinical issue had been resolved. Dr. Haydar makes a generically valid point that clinical research may possibly lead to inattentiveness. However,
© 2015 John Wiley & Sons Ltd Pediatric Anesthesia 25 (2015) 753–760
in our case, distraction from the research protocol could not, and did not, occur. There was no ‘reverse Hawthorne’ effect. Our initial submission did include a root cause analysis and discussion of how to reduce syringe swaps, but the editors asked us to omit this material as the topic is well described in the literature. In short, multiple issues contributed to this particular event: a last-minute change in anesthesiologists; production pressure; equipment set up and medication preparation by multiple individuals; variability in syringe labeling and anesthesia workspace configuration practices among practitioners; bupivacaine not yet programmed into the library of a new label-maker machine; and a visual washout effect of certain drug-label colors against a blue towel. While most of these events are prosaic in current anesthesia practice, in this case they aligned so as to create a unique ‘Swiss cheese’ medical error. As to Dr. Haydar’s question of what systemic changes were actually implemented at our institution after this event, the answer is that a two-person drug readback now occurs before pediatric caudal blockade—a double-check that has also been discussed in the context of other adverse drug events (3). Finally, the reason for the publication delay was to ensure no harm to the child after adequate follow-up. This was perhaps the most valuable part of the report. Ethics approval None required for this manuscript. Funding The study received no external funding. Conflict of interest The authors report no conflict of interest. David A. August & Charles J. Cote Division of Pediatric Anesthesia, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA Email: [email protected] doi:10.1111/pan.12661
753
Correspondence
References 1 August DA, Sui J, Cote CJ. Unintentional epidural injection of 88 lgkg 1 of epinephrine. Pediatr Anesth 2014; 24: 1185–1187.
2 Haydar B. Harm attributable to research distraction? Challenging conclusions on caudal epinephrine. Pediatr Anesth 2014; 24: 1313–1314.
3 O’Connor M. Responsiveness to the chlorhexidine epidural tragedy: a mental block? J Law Med 2012; 19: 436–443.
Craniosynostosis reconstruction in patients with cyanotic heart defects—risk factors for venous air embolism and overview of preventative strategies SIR—We commend the authors, Bergmans et al. (1), for a thoughtful case report of craniosynostosis surgery in an infant with complex congenital heart disease. The judicious replacement of intraoperative blood loss and use of a higher transfusion threshold owing to the patient’s chronic hypoxia and tendency toward polycythemia were indispensable to the success of the operation. While the report addresses crucial issues of perioperative monitoring and hemodynamic management, we would also like to bring attention to a unique perioperative risk in this patient population—the risk of venous air embolism (VAE). Reports of the incidence of VAE during craniosynostosis repair ranges from 8 to 82.6% (2,3). Recognition of VAE is of particular importance in patients with cardiac defects and right-to-left shunts due to the high risk of developing paradoxical arterial emboli. A small amount of air into the cerebral or coronary circulation can be fatal. The patient described had a double outlet right ventricle, multiple ventricular septal defects, atrial septal defect, and transposition of the great vessels. This anatomy placed the patient at risk for arterial emboli due to mixing within the dominant right ventricle and a smaller fraction of pulmonary arterial flow, thereby diminishing the capacity of pulmonary vessels to potentially filter air emboli. In addition, patient positioning during craniofacial and neurosurgical procedures increases the inherent risk of VAE by virtue of the surgical site being elevated above the level of the right atrium. Monitoring for VAE is important and signs of VAE include sudden drop in blood pressure, characteristic change in Doppler tones, decreased endtidal carbon dioxide (ETCO2), increased central venous pressure (CVP), decreased oxygen saturation, right ventricular strain pattern on the EKG, and increased pulmonary artery pressure. In the event that a VAE is suspected, the following measures should be taken (3–5): prompt flooding of the surgical
754
field with saline, continuous monitoring of end-tidal carbon dioxide (ETCO2) and nitrogen (if possible), use of bone wax to prevent entry of atmospheric air, use of precordial Doppler ultrasonography for detection, search for open venous sinuses, and strict intra-arterial blood pressure monitoring. Additional therapeutic maneuvers include aspiration via right atrial catheter and left lateral decubitus or Trendelenburg positioning. Interestingly, this patient’s unique physiology may have potentially reduced the risk of VAE in one respect—the confluence of cardiac defects resulted in an elevated CVP (9–14 mmHg). As jugular venous pressure was already above atmospheric pressure, violation of a vein would favor bleeding instead of air entrainment. Management of patients with comorbid congenital anomalies necessitates the collaboration of multiple disciplines. This approach allows risk reduction with appreciation of each patient’s relevant anatomic and physiologic aberrancies. The occurrence of VAE is exceptionally ominous in patients with cardiac defects, thus intraoperative avoidance, detection, and response are paramount to maximizing patient safety. Communication among all treating specialists is critical both during the time-out process and during the surgical procedure to optimize patient outcomes. Acknowledgments None. Funding The study received no external funding. Conflict of interest The authors report no conflict of interest.
© 2015 John Wiley & Sons Ltd Pediatric Anesthesia 25 (2015) 753–760
