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Facial nerve paralysis during cervical plexus block for carotid artery endarterectomy
782
LETTERS TO THE EDITOR
experience also clearly shows that auscultation and attention to clinical signs must be performed carefully for safe and accurate DLT placement. Jay B. Brodsky, MD Harry J.M. Lemmens, MD, PhD Department of Anesthesia Stanford University School of Medicine Stanford, CA REFERENCES 1. Slinger P: Editorial—A view of and through double-lumen tubes. J Cardiothorac Vasc Anesth 17:287-288, 2003 2. Brodsky JB, Lemmens HJM: Left double-lumen tubes: Experience with 1,170 patients. J Cardiothorac Vasc Anesth 17:289-298, 2003 3. Ching SL, Chow MY, Ng HN: Difficult lung isolation in a patient with an undiagnosed tracheal diverticulum. J Cardiothorac Vasc Anesth 17:355-356, 2003 doi:10.1053/j.jvca.2003.09.027
Hemodynamic Compromise After Bougie Placement To the Editor: Nissen fundoplication is becoming a standard operation for severe gastroesophageal reflux disease. During the final stages of the fundoplication, a bougie is placed into the esophagus to facilitate proper wrapping of the stomach. Over the last 10 years, we have provided anesthesia for more than 500 patients undergoing laparoscopic Nissen fundoplication at our institution. We have seen more than 6 cases of hemodynamic compromise in the form of hypotension and tachycardia during and after bougie placement, which returned to normal once the bougie was removed. Blood pressure drop was in the range of 30 to 40 mmHg systolic and occurred with the use of a 60Fr Bougie. We did not see any hemodynamic alterations with bougies of smaller gauge (48-55Fr). It is possible that the large gauge bougie may compress the left atrium and pulmonary veins, which are directly posterior to the esophagus. In addition, gas insufflation of the abdomen during laparoscopic procedures results in elevation of intraabdominal and intrathoracic pressures, causing reduction in venous return and further aggravating the hemodynamic problems. Pulmonary artery pressures measured by flow directed catheters did not significantly change with the drop in the systemic blood pressures. Therefore, we recommend close monitoring of hemodynamic parameters when placing a large gauge bougie for this procedure. Maggy Riad, MD Duraiyah Thangathurai, MD Peter Roffey, MD Mariana Mogos, MD Maged Mikhail, MD Philip Lumb, MB, BS, FCCM Department of Anesthesiology University of Southern California Los Angeles, CA doi:10.1053/j.jvca.2003.09.025
Facial Nerve Paralysis During Cervical Plexus Block for Carotid Artery Endarterectomy To the Editor: Cervical plexus block is a regional anesthesia frequently used for carotid endarterectomy.1 It facilitates cerebral function monitoring and provides perioperative cardiovascular stability.2 Possible complications include intravascular and intrathecal injection of the local anesthetic and paralysis of the phrenic, the glossopharyngeal, or the hypoglossal nerve.3 We are describing an unreported complication encountered during cervical plexus block. A 70-year-old man was scheduled for a right carotid endarterectomy under cervical plexus block. He had an 80% occlusion of the right internal carotid artery. Significant medical history included coronary artery disease, diabetes, and 50 packs/year of smoking. To perform the deep cervical plexus block, the transverse processes of C2, C3, and C4 were located by drawing a line from the mastoid to the tubercle of Chassaignac and moving down the line 2 cm for each transverse process. Two-inch needles were placed at these processes and 1.5% lidocaine, 7 mL, with epinephrine were injected in each needle to block C2, C3, and C4 nerve roots. The superficial cervical plexus was anesthetized along the posterior border of the sternocleidomastoid muscle with 10 mL of
LETTERS TO THE EDITOR
783
the same solution. Sensory testing indicated the onset of anesthesia in the appropriate nerves distribution, but concomitantly the patient developed paralysis of the right muscles of facial expression. The corner of his mouth dropped, the creases and skin folds were effaced, and the forehead was unfurrowed. The patient was unable to close his right eyelids, and upon trying, his eye rolled upward (Bell phenomena). The patient was fully awake, and no other motor or sensory loss was demonstrable. The diagnosis of facial nerve palsy was made, and surgery was postponed. The clinical signs of facial paralysis started to regress 1 hour later and then disappeared completely. The facial nerve is mainly a motor nerve supplying all the muscles concerned with facial expression on 1 side. It has a course in the skull and exits at the stylomastoid foramen. It then passes through the parotid gland and subdivides to supply the facial muscles. The course of the facial nerve in the neck is anterior to the cervical plexus, and a cervical block is not supposed to reach it. The paralysis of the facial nerve in our case may be explained by the diffusion of lidocaine to the stylomastoid foramen because of inappropriate location of C2 transverse process. Another possible cause is the injection of local anesthetic along the posterior border of the sternocleidomastoid muscle up to the mastoid process. In conclusion, temporary facial nerve paralysis may be encountered during cervical plexus block and should not be mistaken for a cerebral ischemic attack. This complication is avoided by appropriate location of C2 transverse process and by not injecting local anesthetics up to the mastoid process. Gemma Hayek, MD Alexandre Yazigi, MD Samia Jebara, MD Fadia Haddad, MD Nathalie Rokeibi, MD Department of Anesthesia and Intensive Care Hotel-Dieu de France Hospital Saint Joseph University Beirut, Lebanon REFERENCES 1. Davies MJ, Silbert BS, Scott DA, et al: Superficial and deep cervical plexus block for carotid artery surgery: A prospective study of 1000 blocks. Reg Anesth 22:442-446, 1997 2. David A, Zvara MD: Regional anesthesia is the best technique for carotid endarterectomy. J Cardiothorac Vasc Anesth 12:111-114, 1998 3. Germain H: L’anesthe´ sie re´ gionale de la teˆ te et du cou, in Gauthier-Lafaye P (ed): Pre´ cis d’anesthe´ sie loco-re´ gionale. Paris, France, Masson, 1994, pp 71- 89 doi:10.1053/j.jvca.2003.09.028
The Use of Nitric Oxide as Part of the Sweep Gas Infusion During Cardiopulmonary Bypass To the Editor: The increased bleeding tendency after cardiopulmonary bypass (CPB) is in part attributed to platelet dysfunction and thrombocytopenia induced by the CPB circuit. Nitric oxide (NO) inhibits platelet activation and aggregation by elevating 3, 5-cyclic guanosine monophosphate levels in platelets.1 Recent interest has focused on the ability of NO to inhibit platelet activation and aggregation during CPB when administered to the membrane oxygenator unit as part of the sweep gas infusion. Despite encouraging results in vitro,2 in vivo work has produced contradictory results.3,4 However, in the studies to date, the concentration of NO has been measured in the sweep gas infusion but not on the blood side of the membrane oxygenator. NO is a highly unstable molecule with a half-life of a few seconds, and a delay in NO reaching and permeating the membrane oxygenator may result in degradation and loss of its biological actions. We investigated the concentration of NO on either side of the membrane oxygenator at different NO flow rates to see if this was a confounding factor that may alter the effective NO concentration and explain the contradictory results of other studies. A COBE CML Duo oxygenator (COBE Cardiovascular Inc, Arvada, CO) was set up to receive a sweep gas infusion of NO (BOC Limited, Guildford, United Kingdom) with a certified concentration of 422 ppb. By using a flow regulator graduated in liters per minute, we were able to vary the flow of NO delivered to the oxygenator unit. Analysis of NO concentration was performed by using a NO analyzer (Logan Research Limited, Rochester, UK), with an accuracy of ⫾ 0.3 ppb. The sampling port was within 30 cm of the membrane oxygenator. The blood circuit was run “dry” to simplify the sampling process. The blood inflow was closed, and sampling of NO was from the blood outflow circuit. Once again, the sampling port was within 30 cm of the membrane oxygenator to get an accurate value for NO concentration at the membrane oxygenator/blood interface. Our results show that at sweep gas flow rates of 1 and 2 L/min, the concentration of NO on the blood side of the membrane oxygenator is significantly less (258 ppb and 276 ppb, respectively) than its concentration in the infused gas (410 ppb). Above a flow of 3 L/min, there was equilibrium between both sides of the membrane. This would suggest that the membrane oxygenator
LETTERS TO THE EDITOR
experience also clearly shows that auscultation and attention to clinical signs must be performed carefully for safe and accurate DLT placement. Jay B. Brodsky, MD Harry J.M. Lemmens, MD, PhD Department of Anesthesia Stanford University School of Medicine Stanford, CA REFERENCES 1. Slinger P: Editorial—A view of and through double-lumen tubes. J Cardiothorac Vasc Anesth 17:287-288, 2003 2. Brodsky JB, Lemmens HJM: Left double-lumen tubes: Experience with 1,170 patients. J Cardiothorac Vasc Anesth 17:289-298, 2003 3. Ching SL, Chow MY, Ng HN: Difficult lung isolation in a patient with an undiagnosed tracheal diverticulum. J Cardiothorac Vasc Anesth 17:355-356, 2003 doi:10.1053/j.jvca.2003.09.027
Hemodynamic Compromise After Bougie Placement To the Editor: Nissen fundoplication is becoming a standard operation for severe gastroesophageal reflux disease. During the final stages of the fundoplication, a bougie is placed into the esophagus to facilitate proper wrapping of the stomach. Over the last 10 years, we have provided anesthesia for more than 500 patients undergoing laparoscopic Nissen fundoplication at our institution. We have seen more than 6 cases of hemodynamic compromise in the form of hypotension and tachycardia during and after bougie placement, which returned to normal once the bougie was removed. Blood pressure drop was in the range of 30 to 40 mmHg systolic and occurred with the use of a 60Fr Bougie. We did not see any hemodynamic alterations with bougies of smaller gauge (48-55Fr). It is possible that the large gauge bougie may compress the left atrium and pulmonary veins, which are directly posterior to the esophagus. In addition, gas insufflation of the abdomen during laparoscopic procedures results in elevation of intraabdominal and intrathoracic pressures, causing reduction in venous return and further aggravating the hemodynamic problems. Pulmonary artery pressures measured by flow directed catheters did not significantly change with the drop in the systemic blood pressures. Therefore, we recommend close monitoring of hemodynamic parameters when placing a large gauge bougie for this procedure. Maggy Riad, MD Duraiyah Thangathurai, MD Peter Roffey, MD Mariana Mogos, MD Maged Mikhail, MD Philip Lumb, MB, BS, FCCM Department of Anesthesiology University of Southern California Los Angeles, CA doi:10.1053/j.jvca.2003.09.025
Facial Nerve Paralysis During Cervical Plexus Block for Carotid Artery Endarterectomy To the Editor: Cervical plexus block is a regional anesthesia frequently used for carotid endarterectomy.1 It facilitates cerebral function monitoring and provides perioperative cardiovascular stability.2 Possible complications include intravascular and intrathecal injection of the local anesthetic and paralysis of the phrenic, the glossopharyngeal, or the hypoglossal nerve.3 We are describing an unreported complication encountered during cervical plexus block. A 70-year-old man was scheduled for a right carotid endarterectomy under cervical plexus block. He had an 80% occlusion of the right internal carotid artery. Significant medical history included coronary artery disease, diabetes, and 50 packs/year of smoking. To perform the deep cervical plexus block, the transverse processes of C2, C3, and C4 were located by drawing a line from the mastoid to the tubercle of Chassaignac and moving down the line 2 cm for each transverse process. Two-inch needles were placed at these processes and 1.5% lidocaine, 7 mL, with epinephrine were injected in each needle to block C2, C3, and C4 nerve roots. The superficial cervical plexus was anesthetized along the posterior border of the sternocleidomastoid muscle with 10 mL of
LETTERS TO THE EDITOR
783
the same solution. Sensory testing indicated the onset of anesthesia in the appropriate nerves distribution, but concomitantly the patient developed paralysis of the right muscles of facial expression. The corner of his mouth dropped, the creases and skin folds were effaced, and the forehead was unfurrowed. The patient was unable to close his right eyelids, and upon trying, his eye rolled upward (Bell phenomena). The patient was fully awake, and no other motor or sensory loss was demonstrable. The diagnosis of facial nerve palsy was made, and surgery was postponed. The clinical signs of facial paralysis started to regress 1 hour later and then disappeared completely. The facial nerve is mainly a motor nerve supplying all the muscles concerned with facial expression on 1 side. It has a course in the skull and exits at the stylomastoid foramen. It then passes through the parotid gland and subdivides to supply the facial muscles. The course of the facial nerve in the neck is anterior to the cervical plexus, and a cervical block is not supposed to reach it. The paralysis of the facial nerve in our case may be explained by the diffusion of lidocaine to the stylomastoid foramen because of inappropriate location of C2 transverse process. Another possible cause is the injection of local anesthetic along the posterior border of the sternocleidomastoid muscle up to the mastoid process. In conclusion, temporary facial nerve paralysis may be encountered during cervical plexus block and should not be mistaken for a cerebral ischemic attack. This complication is avoided by appropriate location of C2 transverse process and by not injecting local anesthetics up to the mastoid process. Gemma Hayek, MD Alexandre Yazigi, MD Samia Jebara, MD Fadia Haddad, MD Nathalie Rokeibi, MD Department of Anesthesia and Intensive Care Hotel-Dieu de France Hospital Saint Joseph University Beirut, Lebanon REFERENCES 1. Davies MJ, Silbert BS, Scott DA, et al: Superficial and deep cervical plexus block for carotid artery surgery: A prospective study of 1000 blocks. Reg Anesth 22:442-446, 1997 2. David A, Zvara MD: Regional anesthesia is the best technique for carotid endarterectomy. J Cardiothorac Vasc Anesth 12:111-114, 1998 3. Germain H: L’anesthe´ sie re´ gionale de la teˆ te et du cou, in Gauthier-Lafaye P (ed): Pre´ cis d’anesthe´ sie loco-re´ gionale. Paris, France, Masson, 1994, pp 71- 89 doi:10.1053/j.jvca.2003.09.028
The Use of Nitric Oxide as Part of the Sweep Gas Infusion During Cardiopulmonary Bypass To the Editor: The increased bleeding tendency after cardiopulmonary bypass (CPB) is in part attributed to platelet dysfunction and thrombocytopenia induced by the CPB circuit. Nitric oxide (NO) inhibits platelet activation and aggregation by elevating 3, 5-cyclic guanosine monophosphate levels in platelets.1 Recent interest has focused on the ability of NO to inhibit platelet activation and aggregation during CPB when administered to the membrane oxygenator unit as part of the sweep gas infusion. Despite encouraging results in vitro,2 in vivo work has produced contradictory results.3,4 However, in the studies to date, the concentration of NO has been measured in the sweep gas infusion but not on the blood side of the membrane oxygenator. NO is a highly unstable molecule with a half-life of a few seconds, and a delay in NO reaching and permeating the membrane oxygenator may result in degradation and loss of its biological actions. We investigated the concentration of NO on either side of the membrane oxygenator at different NO flow rates to see if this was a confounding factor that may alter the effective NO concentration and explain the contradictory results of other studies. A COBE CML Duo oxygenator (COBE Cardiovascular Inc, Arvada, CO) was set up to receive a sweep gas infusion of NO (BOC Limited, Guildford, United Kingdom) with a certified concentration of 422 ppb. By using a flow regulator graduated in liters per minute, we were able to vary the flow of NO delivered to the oxygenator unit. Analysis of NO concentration was performed by using a NO analyzer (Logan Research Limited, Rochester, UK), with an accuracy of ⫾ 0.3 ppb. The sampling port was within 30 cm of the membrane oxygenator. The blood circuit was run “dry” to simplify the sampling process. The blood inflow was closed, and sampling of NO was from the blood outflow circuit. Once again, the sampling port was within 30 cm of the membrane oxygenator to get an accurate value for NO concentration at the membrane oxygenator/blood interface. Our results show that at sweep gas flow rates of 1 and 2 L/min, the concentration of NO on the blood side of the membrane oxygenator is significantly less (258 ppb and 276 ppb, respectively) than its concentration in the infused gas (410 ppb). Above a flow of 3 L/min, there was equilibrium between both sides of the membrane. This would suggest that the membrane oxygenator