Correspondence
variety of reasons. Migration of the tracheal tube may occur after correct placement and result from movement of the patient’s head and/or neck or general repositioning of the patient.1,2 Neck extension has been shown to be associated with movement of the tube tip up to 5.2 cm away from the carina.3 Hartrey and Kestin4 have shown that both nasal and orotracheal tubes move an average of 15 mm toward the carina with head and neck flexion and 8.5 mm away with extension. However, in this case, endobronchial intubation was not because of neck movements, but rather owing to the corrective procedure resulting in decreased relative length, which the anesthesiologist has to keep in mind. Himanshu Goyal, MD Girija P. Rath, MD, DM Department of Neuroanaesthesiology All India Institute of Medical Sciences (AIIMS), New Delhi, India
REFERENCES 1. McCoy EP, Russell WJ, Webb RK. Accidental bronchial intubation. An analysis of AIMS incident reports from 1988 to 1994 inclusive. Anaesthesia. 1997;52:24–31. 2. Riley RH, Marcey JH. Unsuspected endobronchial intubation—detection by continuous mass spectrometry. Anesthesiology. 1985; 63:203–204. 3. Conrardy PA, Goodman LR, Lainge F, et al. Alteration of endotracheal tube position with flexion and extension of the neck. Crit Care Med. 1976;4:8–12. 4. Hartrey R, Kestin IG. Movement of oral and nasal tracheal tubes as a result of changes in head and neck position. Anaesthesia. 1995;50:682–687.
Therapeutic Hypothermia After Cardiac Arrest During Craniotomy To JNA Readers: Therapeutic hypothermia has been shown to be beneficial in comatose survivors after cardiac arrest.1 The authors have no funding or conflicts of interest to disclose.
70 | www.jnsa.com
J Neurosurg Anesthesiol
Recent surgery is a relative contraindication, due to the risk of bleeding. We report a woman who received therapeutic hypothermia after a supratentorial craniotomy. A woman, 41 years old with antecedents of obesity (body mass index = 37), diagnosed with left paramedian meningioma of which the only symptom was headache. She was scheduled for craniotomy and exeresis of meningioma. The patient was monitored using ECG, invasive blood pressure, pulse oximetry (Dra¨ger Cicero PM8060; Dra¨ger Medical, Lu¨beck, Germany). A 3-lumen internal jugular venous catheter was placed (Arrow; Arrow International, Bernville, PA). Anesthesia was administered with continuous intravenous propofol, remifentanil, and cisatracurium. After anesthetic induction, the patient was placed in the supine position with the head elevated 30 degrees using a Mayfield 3-pin holder. Resection of the tumor was unremarkable. At the end of the surgery, at the same time as the closing of the subcutaneous tissue, the patient suffered arterial hypotension, sudden drop in ETCO2, extreme bradycardia, and immediate ventricular fibrillation. After 15 minutes of advanced cardiac life support, a sinus rhythm was obtained. She was taken to the ICU. A cerebral computed tomography was performed, ruling out hemorrhage and signs of endocranial hypertension. Therefore, a transthoracic echocardiogram was carried out, which demonstrated good ventricular function and the absence of oval foramen. After removing the sedation, we confirmed that the patient did not respond to verbal commands and only opened her eyes when a painful stimulus was applied. After 4 hours of cardiac arrest and with a presumed diagnosis of air embolism, therapeutic hypothermia was established at 331C using intravascular cooling system Cool-Gard3000 (Zoll, Chelmsford, MA). The warming velocity was 11C to 1.31C per hour. The patient was administered propofol and cisatracurium for the purpose of sedation and neuromuscular block for 24 hours. Afterwards, a gradual rewarming was achieved, raising the temper-
Volume 27, Number 1, January 2015
ature between 0.21C and 0.51C per hour, reaching 361C. During both the induction and maintenance of hypothermia and the rewarming, there were no hydroelectrolytic or hemodynamic complications, and no signs of hemorrhage. After the removal of sedation and neuromuscular block, the patient responded to simple verbal commands with spontaneous opening of the eyes. The patient was extubated without incident, and at 48 hours she was transferred to the ward with a glasgow coma score of 15 with no focal deficits noted on neurological examination. Therapeutic hypothermia after cardiac arrest is indicated especially in cardiac arrest with defibrillation rhythms outside the hospital. However, it is also acceptable after in-hospital cardiac arrest. Although recent major surgery is a relative contraindication for therapeutic hypothermia due to the risk of bleeding, there are published cases after cardiac surgery.2 As far as we know, this is the first published case of induced hypothermia soon after craniotomy. In patients with low intracranial compliance, minimal hemorrhage can cause irreparable neurological damage. Nevertheless, it is precisely in these patients that anoxia during cardiac arrest and reperfusion syndrome can aggravate preexisting neurological damage. In this way, therapeutic hypothermia decreases cellular apoptosis, reducing the liberation of excitatory amino acids and free radicals. Moreover, it reduces cerebral metabolism and intracranial pressure, improving the balance between supply and demand of cerebral oxygen. In our case, therapeutic hypothermia was effective and the patient’s outcome was good. We believe that therapeutic hypothermia may be especially beneficial in the neurosurgery patient. Up to now, scientific knowledge does not consider this practice safe and efficient, but we believe the suitability of using therapeutic hypothermia should be considered in patients without the risk for coagulopathy, cerebral hemorrhage, active bleeding, or severe arrhythmias. Lucı´ a Valencia, MD Aurelio Rodrı´ guez-Pe´rez, MD Cesar Barajas-Fontecha, MD r
2014 Lippincott Williams & Wilkins
J Neurosurg Anesthesiol
Volume 27, Number 1, January 2015
Hospital Universitario de Gran Canaria Doctor Negrı´ n, Spain
REFERENCES 1. Morrison LJ, Neumar RW, Zimmerman JL, et al. Strategies for improving survival after inhospital cardiac arrest in the United States: 2013 consensus recommendations: a consensus statement from the American Heart Association. Circulation. 2013;127:1538–1563. 2. Rinehart TW, Merkel MJ, Schulman PM, et al. Therapeutic hypothermia after perioperative cardiac arrest in cardiac surgical patients. ICU Dir. 2012;3:271–278.
Intra-arterial Etomidate for Provocative Testing in Embolization Procedure for Cerebral Arteriovenous Malformation To JNA Readers: The treatment of cerebral arteriovenous malformations (AVMs) by endovascular techniques is of value in the overall management of AVMs. However, ischemic deficits secondary to embolization or compromise of arterial supply to normal brain regions can be seen in 10% and 50% of the treated patients.1 Injection of anesthetic agent before embolization of an arterial feeder of an AVM followed by a neurological examination to detect any new deficits (provocative test) is typically performed. Absence of any new neurological deficits confirms the absence of risk to normal brain region.2 Short-acting barbiturates for intracranial lesions and lidocaine for extracranial lesions have been used as intra-arterial injections. Amobarbital has been the traditional drug of choice for preembolization testing; yet, its availability and limitations have prompted many centers to consider the use of other drugs. Several agents have been used as intracarotid injections for WADA The authors have no funding or conflicts of interest to disclose. r
2014 Lippincott Williams & Wilkins
testing including methohexital, pentobarbital, etomidate, and propofol. Although etomidate has been used with good results for WADA testing,3 use of etomidate has not been described for provocative testing before cerebral AVM embolization. Etomidate is a short-acting intravenous anesthetic agent used for the induction of general anesthesia and for sedation for short procedures, such as reduction of dislocated joints, tracheal intubation, and cardioversion.4 We report our experience with the use of etomidate for provocative testing before AVM embolization. A 62-year-old hypertensive man presented with headache and left homonymous hemianopsia associated with right parietal-occipital intraparenchymal hemorrhage. A cerebral angiogram demonstrated a 36 mm 16 mm right parieto-occipital AVM with prenidal aneurysm. The arterial contribution was predominantly from cortical branches of middle cerebral artery. Venous outflow was through cortical veins into superior sagittal sinus and Vein of Galen into the straight sinus. Subsequently, embolization was planned in awake state and a microcatheter was placed in the arterial feeder from inferior division of right middle cerebral artery. To determine the contribution of the arteries and arterioles distal to the microcatheter tip, we sequentially injected 1 mg of etomidate (2 mg in 4 mL 0.9% NaCl); 3 mg of methohexital (brevital, 1 mg/mL); and 20 mg of lidocaine (1% solution). Each of the agents was injected over a period of 1 minute and separated by at least 5 minutes. We performed neurological examination before and after (at 1 and 5 min) each injection using the endovascular procedure-specific scheme (NES), which evaluates 6 aspects of neurological function, including language, gaze deviation, visual fields, cranial nerves, and the function of the upper lower extremities (left and right) as described previously.5 We monitored the BP using automated cuff measurements every 3 minutes. Heart rate and oxygen saturation were monitored continuously. We did not observe any new neurological deficits after in-
Correspondence
jection of any of the 3 agents. All 3 agents did not result in any alteration in hemodynamic status or level of consciousness. The 1 mg dose was selected based on the dose used in WADA testing (2 mg followed by an infusion of 10 mg/kg/min).6 As only a focal segment of hemisphere is evaluated for testing in a cerebral AVM and 2 mg would result in suppression of hemispheric function, we decided to select a 1 mg dose of etomidate. Following testing, Onyx injection was started at a rate of 0.1 mL/min. The embolic agent was released at the tip of microcatheter under free-flow conditions and filled the directly dependent nidus compartment in an anterograde and later retrograde manner, until it flowed to the tip of the microcatheter as described previously.5 A neurological examination immediate and 24-hour postprocedure did not reveal any new neurological deficits, confirming the validity of the provocative testing. Intra-arterial etomidate can be used in low doses as a provocative test before embolization of cerebral AVMs similar to other agents. Naseeb Ullah, MBBS*w Asif A. Khan, MD*w Muhammad F. K. Suri, MD*w Adnan I. Qureshi, MD*w *Zeenat Qureshi Stroke Institute wDepartment of Cerebrovascular Diseases and Interventional Neurology CentraCare Health, Saint Cloud Hospital Saint Cloud, MN
REFERENCES 1. Qureshi AI, Luft AR, Sharma M, et al. Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: part ii—clinical aspects and recommendations. Neurosurgery. 2000;46:1360–1375; discussion 1375-1366. 2. Barr JD, Mathis JM, Horton JA. Provocative pharmacologic testing during arterial embolization. Neurosurg Clin N Am. 1994; 5:403–411. 3. Patel A, Wordell C, Szarlej D. Alternatives to sodium amobarbital in the wada test. Ann Pharmacother. 2011;45:395–401. 4. Vinson DR, Bradbury DR. Etomidate for procedural sedation in emergency medicine. Ann Emerg Med. 2002;39:592–598. 5. Natarajan SK, Ghodke B, Britz GW, et al. Multimodality treatment of brain arteriovenous malformations with microsurgery after embolization with onyx: single-center experience and technical nuances. Neurosurgery. 2008;62:1213–1225; discussion 1225-1216.
www.jnsa.com |
71
variety of reasons. Migration of the tracheal tube may occur after correct placement and result from movement of the patient’s head and/or neck or general repositioning of the patient.1,2 Neck extension has been shown to be associated with movement of the tube tip up to 5.2 cm away from the carina.3 Hartrey and Kestin4 have shown that both nasal and orotracheal tubes move an average of 15 mm toward the carina with head and neck flexion and 8.5 mm away with extension. However, in this case, endobronchial intubation was not because of neck movements, but rather owing to the corrective procedure resulting in decreased relative length, which the anesthesiologist has to keep in mind. Himanshu Goyal, MD Girija P. Rath, MD, DM Department of Neuroanaesthesiology All India Institute of Medical Sciences (AIIMS), New Delhi, India
REFERENCES 1. McCoy EP, Russell WJ, Webb RK. Accidental bronchial intubation. An analysis of AIMS incident reports from 1988 to 1994 inclusive. Anaesthesia. 1997;52:24–31. 2. Riley RH, Marcey JH. Unsuspected endobronchial intubation—detection by continuous mass spectrometry. Anesthesiology. 1985; 63:203–204. 3. Conrardy PA, Goodman LR, Lainge F, et al. Alteration of endotracheal tube position with flexion and extension of the neck. Crit Care Med. 1976;4:8–12. 4. Hartrey R, Kestin IG. Movement of oral and nasal tracheal tubes as a result of changes in head and neck position. Anaesthesia. 1995;50:682–687.
Therapeutic Hypothermia After Cardiac Arrest During Craniotomy To JNA Readers: Therapeutic hypothermia has been shown to be beneficial in comatose survivors after cardiac arrest.1 The authors have no funding or conflicts of interest to disclose.
70 | www.jnsa.com
J Neurosurg Anesthesiol
Recent surgery is a relative contraindication, due to the risk of bleeding. We report a woman who received therapeutic hypothermia after a supratentorial craniotomy. A woman, 41 years old with antecedents of obesity (body mass index = 37), diagnosed with left paramedian meningioma of which the only symptom was headache. She was scheduled for craniotomy and exeresis of meningioma. The patient was monitored using ECG, invasive blood pressure, pulse oximetry (Dra¨ger Cicero PM8060; Dra¨ger Medical, Lu¨beck, Germany). A 3-lumen internal jugular venous catheter was placed (Arrow; Arrow International, Bernville, PA). Anesthesia was administered with continuous intravenous propofol, remifentanil, and cisatracurium. After anesthetic induction, the patient was placed in the supine position with the head elevated 30 degrees using a Mayfield 3-pin holder. Resection of the tumor was unremarkable. At the end of the surgery, at the same time as the closing of the subcutaneous tissue, the patient suffered arterial hypotension, sudden drop in ETCO2, extreme bradycardia, and immediate ventricular fibrillation. After 15 minutes of advanced cardiac life support, a sinus rhythm was obtained. She was taken to the ICU. A cerebral computed tomography was performed, ruling out hemorrhage and signs of endocranial hypertension. Therefore, a transthoracic echocardiogram was carried out, which demonstrated good ventricular function and the absence of oval foramen. After removing the sedation, we confirmed that the patient did not respond to verbal commands and only opened her eyes when a painful stimulus was applied. After 4 hours of cardiac arrest and with a presumed diagnosis of air embolism, therapeutic hypothermia was established at 331C using intravascular cooling system Cool-Gard3000 (Zoll, Chelmsford, MA). The warming velocity was 11C to 1.31C per hour. The patient was administered propofol and cisatracurium for the purpose of sedation and neuromuscular block for 24 hours. Afterwards, a gradual rewarming was achieved, raising the temper-
Volume 27, Number 1, January 2015
ature between 0.21C and 0.51C per hour, reaching 361C. During both the induction and maintenance of hypothermia and the rewarming, there were no hydroelectrolytic or hemodynamic complications, and no signs of hemorrhage. After the removal of sedation and neuromuscular block, the patient responded to simple verbal commands with spontaneous opening of the eyes. The patient was extubated without incident, and at 48 hours she was transferred to the ward with a glasgow coma score of 15 with no focal deficits noted on neurological examination. Therapeutic hypothermia after cardiac arrest is indicated especially in cardiac arrest with defibrillation rhythms outside the hospital. However, it is also acceptable after in-hospital cardiac arrest. Although recent major surgery is a relative contraindication for therapeutic hypothermia due to the risk of bleeding, there are published cases after cardiac surgery.2 As far as we know, this is the first published case of induced hypothermia soon after craniotomy. In patients with low intracranial compliance, minimal hemorrhage can cause irreparable neurological damage. Nevertheless, it is precisely in these patients that anoxia during cardiac arrest and reperfusion syndrome can aggravate preexisting neurological damage. In this way, therapeutic hypothermia decreases cellular apoptosis, reducing the liberation of excitatory amino acids and free radicals. Moreover, it reduces cerebral metabolism and intracranial pressure, improving the balance between supply and demand of cerebral oxygen. In our case, therapeutic hypothermia was effective and the patient’s outcome was good. We believe that therapeutic hypothermia may be especially beneficial in the neurosurgery patient. Up to now, scientific knowledge does not consider this practice safe and efficient, but we believe the suitability of using therapeutic hypothermia should be considered in patients without the risk for coagulopathy, cerebral hemorrhage, active bleeding, or severe arrhythmias. Lucı´ a Valencia, MD Aurelio Rodrı´ guez-Pe´rez, MD Cesar Barajas-Fontecha, MD r
2014 Lippincott Williams & Wilkins
J Neurosurg Anesthesiol
Volume 27, Number 1, January 2015
Hospital Universitario de Gran Canaria Doctor Negrı´ n, Spain
REFERENCES 1. Morrison LJ, Neumar RW, Zimmerman JL, et al. Strategies for improving survival after inhospital cardiac arrest in the United States: 2013 consensus recommendations: a consensus statement from the American Heart Association. Circulation. 2013;127:1538–1563. 2. Rinehart TW, Merkel MJ, Schulman PM, et al. Therapeutic hypothermia after perioperative cardiac arrest in cardiac surgical patients. ICU Dir. 2012;3:271–278.
Intra-arterial Etomidate for Provocative Testing in Embolization Procedure for Cerebral Arteriovenous Malformation To JNA Readers: The treatment of cerebral arteriovenous malformations (AVMs) by endovascular techniques is of value in the overall management of AVMs. However, ischemic deficits secondary to embolization or compromise of arterial supply to normal brain regions can be seen in 10% and 50% of the treated patients.1 Injection of anesthetic agent before embolization of an arterial feeder of an AVM followed by a neurological examination to detect any new deficits (provocative test) is typically performed. Absence of any new neurological deficits confirms the absence of risk to normal brain region.2 Short-acting barbiturates for intracranial lesions and lidocaine for extracranial lesions have been used as intra-arterial injections. Amobarbital has been the traditional drug of choice for preembolization testing; yet, its availability and limitations have prompted many centers to consider the use of other drugs. Several agents have been used as intracarotid injections for WADA The authors have no funding or conflicts of interest to disclose. r
2014 Lippincott Williams & Wilkins
testing including methohexital, pentobarbital, etomidate, and propofol. Although etomidate has been used with good results for WADA testing,3 use of etomidate has not been described for provocative testing before cerebral AVM embolization. Etomidate is a short-acting intravenous anesthetic agent used for the induction of general anesthesia and for sedation for short procedures, such as reduction of dislocated joints, tracheal intubation, and cardioversion.4 We report our experience with the use of etomidate for provocative testing before AVM embolization. A 62-year-old hypertensive man presented with headache and left homonymous hemianopsia associated with right parietal-occipital intraparenchymal hemorrhage. A cerebral angiogram demonstrated a 36 mm 16 mm right parieto-occipital AVM with prenidal aneurysm. The arterial contribution was predominantly from cortical branches of middle cerebral artery. Venous outflow was through cortical veins into superior sagittal sinus and Vein of Galen into the straight sinus. Subsequently, embolization was planned in awake state and a microcatheter was placed in the arterial feeder from inferior division of right middle cerebral artery. To determine the contribution of the arteries and arterioles distal to the microcatheter tip, we sequentially injected 1 mg of etomidate (2 mg in 4 mL 0.9% NaCl); 3 mg of methohexital (brevital, 1 mg/mL); and 20 mg of lidocaine (1% solution). Each of the agents was injected over a period of 1 minute and separated by at least 5 minutes. We performed neurological examination before and after (at 1 and 5 min) each injection using the endovascular procedure-specific scheme (NES), which evaluates 6 aspects of neurological function, including language, gaze deviation, visual fields, cranial nerves, and the function of the upper lower extremities (left and right) as described previously.5 We monitored the BP using automated cuff measurements every 3 minutes. Heart rate and oxygen saturation were monitored continuously. We did not observe any new neurological deficits after in-
Correspondence
jection of any of the 3 agents. All 3 agents did not result in any alteration in hemodynamic status or level of consciousness. The 1 mg dose was selected based on the dose used in WADA testing (2 mg followed by an infusion of 10 mg/kg/min).6 As only a focal segment of hemisphere is evaluated for testing in a cerebral AVM and 2 mg would result in suppression of hemispheric function, we decided to select a 1 mg dose of etomidate. Following testing, Onyx injection was started at a rate of 0.1 mL/min. The embolic agent was released at the tip of microcatheter under free-flow conditions and filled the directly dependent nidus compartment in an anterograde and later retrograde manner, until it flowed to the tip of the microcatheter as described previously.5 A neurological examination immediate and 24-hour postprocedure did not reveal any new neurological deficits, confirming the validity of the provocative testing. Intra-arterial etomidate can be used in low doses as a provocative test before embolization of cerebral AVMs similar to other agents. Naseeb Ullah, MBBS*w Asif A. Khan, MD*w Muhammad F. K. Suri, MD*w Adnan I. Qureshi, MD*w *Zeenat Qureshi Stroke Institute wDepartment of Cerebrovascular Diseases and Interventional Neurology CentraCare Health, Saint Cloud Hospital Saint Cloud, MN
REFERENCES 1. Qureshi AI, Luft AR, Sharma M, et al. Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: part ii—clinical aspects and recommendations. Neurosurgery. 2000;46:1360–1375; discussion 1375-1366. 2. Barr JD, Mathis JM, Horton JA. Provocative pharmacologic testing during arterial embolization. Neurosurg Clin N Am. 1994; 5:403–411. 3. Patel A, Wordell C, Szarlej D. Alternatives to sodium amobarbital in the wada test. Ann Pharmacother. 2011;45:395–401. 4. Vinson DR, Bradbury DR. Etomidate for procedural sedation in emergency medicine. Ann Emerg Med. 2002;39:592–598. 5. Natarajan SK, Ghodke B, Britz GW, et al. Multimodality treatment of brain arteriovenous malformations with microsurgery after embolization with onyx: single-center experience and technical nuances. Neurosurgery. 2008;62:1213–1225; discussion 1225-1216.
www.jnsa.com |
71
