Letters to Editor
likely. The level of sensory block had also receded to T10 by that time. We therefore speculate that a centrally mediated decrease in sympathetic outflow and increase in parasympathetic outflow due to dexmedetomidine may be the cause. The patient’s autonomic response to peritoneal stretching could also be a contributing factor responsible for the severe bradycardia in this case. However, the bradycardia did not respond to the cessation of surgical handling and the usual dose of atropine. A fall in blood pressure and heart rate has been reported with various interventions like displacement of liver, insertion of hand into the peritoneal cavity, placement of packing and retraction of the wound edges. A vagally mediated reflex has been implicated in most cases, but exact pathways have not been established so far.[6] To conclude, although dexmedetomidine is an attractive intrathecal adjuvant for post-operative analgesia, we recommend meticulous use of this drug with vigilant monitoring in the operating room as well as in the post-anaesthesia care unit keeping in mind the possibility of delayed occurrence of severe bradycardia.
Tripat Kaur Bindra, Simarjot Singh Sarin1, Ruchi Gupta, Shubhdeep Departments of Anaesthesia and Critical Care and 1Cardiology, Sri Guru Ram Das Institute of Medical Sciences and Research, Sri Amritsar, Punjab, India Address for correspondence: Dr. Tripat Kaur Bindra, 4735A, Guru Nanak Wara, Amritsar, Punjab, India. E-mail: [email protected]
REFERENCES 1.
Al-Mustafa MM, Abu-Halaweh SA, Aloweidi AS, Murshidi MM, Ammari BA, Awwad ZM, et al. Effect of dexmedetomidine added to spinal bupivacaine for urological procedures. Saudi Med J 2009;30:365-70. 2. Bharati S, Pal A, Biswas C, Biswas R. Incidence of cardiac arrest increases with the indiscriminate use of dexmedetomidine: A case series and review of published case reports. Acta Anaesthesiol Taiwan 2011;49:165-7. 3. Ingersoll-Weng E, Manecke GR Jr, Thistlethwaite PA. Dexmedetomidine and cardiac arrest. Anesthesiology 2004;100:738-9. 4. Kanazi GE, Aouad MT, Jabbour-Khoury SI, Al Jazzar MD, Alameddine MM, Al-Yaman R, et al. Effect of low-dose dexmedetomidine or clonidine on the characteristics of bupivacaine spinal block. Acta Anaesthesiol Scand 2006;50:222-7. 5. Gupta R, Bogra J, Verma R, Kohli M, Kushwaha JK, Kumar S. Dexmedetomidine as an intrathecal adjuvant for postoperative analgesia. Indian J Anaesth 2011;55:347-51. 6. Doyle DJ, Mark PW. Reflex bradycardia during surgery. Can J Anaesth 1990;37:219-22. 228
Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.130851
Anaesthetic management of a case of distal myopathy Sir, Congenital myopathies are a group of rare genetic disorders characterized by a defect in the contractile apparatus of the myocytes.[1] We describe the case of a patient with distal myopathy taken up for total abdominal hysterectomy under general anesthesia as patient refused for neuraxial blockade. A 36‑years‑old female patient diagnosed to have abdominal leiomyosarcoma was planned for total abdominal hysterectomy under general anesthesia. On evaluation the patient gave a history of progressive weakness and thinning of distal aspect of both upper and lower limbs for the last 10 years. She had not sought any medical attention for these complaints. On examination, she was thin built with a BMI of 20. She was haemodynamically stable and had an adequate airway. She had atrophy of distal hand muscles with bilateral claw hands. She also had bilateral foot drop with a high stepping gait [Figure 1a and b]. Deep tendon reflexes, sensory nervous system, cranial nerves and spine examination were normal. Her routine investigations, chest X‑ray and ECG were normal. Electrophysiological studies were suggestive of distal myopathy with normal proximal muscles and sensory system.
a
b
Figure 1: Distal myopathy (with clawing of hand and foot drop) (a) Clawing of hand. (b) Foot drop Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
Letters to Editor
Tab. alprazolam 0.25 mg was given the night before the surgery and adequate blood products were arranged. In the operation theatre, before taking the patient in, all vapourizers were removed from anaesthesia workstation. Soda lime, breathing circuit and face mask were changed. After securing peripheral intravenous line and attaching standard monitors, we started intravenous induction with midazolam 1 mg, fentanyl 60 μcg and 1% propofol 60 mg. After loss of verbal response, we started neuromuscular monitoring with train of four (TOF) and gave atracurium 15 mg. After obtaining no response to TOF, airway was secured with proseal laryngeal mask airway (LMA) of size 3 and post induction monitoring included capnography, nasopharyngeal temperature and TOF count. Maintenance of anesthesia was with with O2/N2O and intravenous propofol infusion at 30-50 µcg/kg/min. Top up doses of atracurium was guided intraoperatively with the TOF count of 3 to achieve adequate muscle relaxation. Haemodynamics and respiratory parameters were maintained within the normal limits throughout the procedure. Thirty minutes before the end of the surgery, diclofenac 1.5 mg/kg and ondansetron 10 µcg/kg were given. At the end of the surgery, neuromuscular blockade was reversed with normal doses of neostigmine and glycopyrrolate and when TOF ratio was ≥0.9, proseal LMA was removed. Post operative period was uneventful. Anaesthetic management of patients with muscle diseases is challenging. In addition to unpredictable sporadic responses, such as rhabdomyolysis and metabolic stimulation, more predictable risks are associated with respiratory and bulbar muscle weakness, myocardial involvement, and difficult airway anatomy. To identify and minimize risk, a thorough preoperative workup is indispensable.[2,3] If regional anesthesia is planned, a preoperative assessment of peripheral sensory nerve dysfunction should be considered. Increased sensitivity to respiratory‑depressant drugs should be anticipated and where possible, doses should be titrated to the desired effect. Even with the most careful anaesthetic management, postoperative ventilatory support may be required and, therefore, postoperative intensive care unit availability should be planned. Baseline serum potassium and creatine kinase (CK) concentrations to assess muscle membrane integrity, family history, cardiac function test and other Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
syndromic features must be sought. It is possible that high baseline values may be associated with increased risk of profound perioperative rhabdomyolysis, whereas the baseline value per se is required to differentiate perioperative rhabdomyolysis from preexisting muscle damage.[3] All anesthetic techniques and drugs are associated with increased risk in patients with myopathies.[4,5] General anaesthesia performed as total intravenous anaesthesia or regional anaesthesia are equally safe. Inhalation agents especially halothane are not recommended because they may trigger a malignant hyperthermia (MH)‑like syndrome.[6] Consideration should be given to the use of short‑acting opioids to avoid the possibility of postoperative ventilation. Use of depolarizing neuromuscular blocking drugs should be generally discouraged in patients with neuromuscular diseases.[4,6] The depolarizing muscle relaxants might trigger MH, and prolonged depolarization leads to potassium release and calcium influx. Although theoretically reversal of neuromuscular block with anticholinesterases in patients with neuromuscular diseases may produce the similar situation, it was not observed in our case. So it can be recommended to use the normal dosage of reversal in such patients. The recent introduction of cyclodextrin reversal drugs (such as sugammadex) provides an attractive alternative in these circumstances. Succinylcholine may also cause acute profound rhabdomyolysis in patients susceptible to MH and those with myopathies. If neuromuscular blockade is required, a non‑depolarizing neuromuscular blocking drug should be used, keeping in mind that patients with myopathies may show increased sensitivity to these drugs. On the basis of cardiac evaluation, there may be an indication for invasive monitoring and use of inotropes in patients with identified cardiac involvement.[5] Strength and range of motion can deteriorate rapidly after surgery and immobilization, and anaesthesia can unmask subclinical respiratory failure.[7] So, patients should be mobilized as soon as possible after surgery.[8]
Neelam Agrawal, Ankur Sharma, Ravindra Batra Department of Anaesthesiology, All India Institute of Medical Sciences (AIIMS), New Delhi, India Address for correspondence: Dr. Ankur Sharma, C/O Mr. Suneel Vyas, C‑2/2287, Vasant Kunj, New Delhi, India. E‑mail: [email protected]
229
Letters to Editor
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8.
Cardamone M, Darras BT, Ryan MM. Inherited myopathies and muscular dystrophies. Semin Neurol 2008;28:250‑9. Nonaka I. Distal myopathies. Curr Opin Neurol 1999;12:493‑9. Klinger W, Rueffert H, Lehmann‑Horn F, Girard T, Hopkins PM. Core myopathies and risk of malignant hyperthermia. Anesth Analg 2009;109:1167‑73. Baraka AS, Jalbout MI. Anesthesia and Myopathy. Curr Opin Anesthesiol 2002;15:371‑6. Farag E, Barsoum S, Spagnuolo S, Tetzlaff J. Anesthesia and muscle disease. The Am J Anesthesiol 2000;27:491‑501. Jones R, Delacourt JL. Muscle rigidity following halothane anaesthesia in two patients with Freeman‑Sheldon Syndrome. Anaesthesiology 1992;77:599‑600. Ryan MM, Ilkovski B, Strickland CD, Schnell C, Sanoudou D, Midgett C, et al. Clinical course correlates poorly withmuscle pathology in nemaline myopathy. Neurology 2003;60:665‑73. Young HK, Lowe A, Fitzgerald DA, Seton C, Waters KA, Kenny E, et al. Non‑invasive ventilation in children with neuromuscular disease: A clinical and quality of life outcome study. Neurology 2007;68:198‑201. Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.130853
All endotracheal tubes that appear endotracheal are not so! Sir, We received a 30‑year‑old man into our intensive care unit who had met with a road traffic accident and suffered head injury. He was referred from another hospital after a resident there intubated him and transported on oxygen supplementation. On examination, the patient was in altered sensorium and agitated (Glasgow Coma Scale E4VTM5). The endotracheal tube (ETT) was fixed at 24 cm mark at the angle of the mouth. He was breathing spontaneously. There was equal movement and air entry on both sides of the chest with respiration. Oxygen saturation of haemoglobin could not be recorded before the administration of sedation as he was agitated. However, gurgling sounds were heard at the mouth. The ETT was connected to a T‑piece to administer oxygen and intravenous sedation was administered. Soon, there was oxygen desaturation even though breathing seemed adequate. An Ambu bag was used to ventilate the patient. It was evident immediately that the ETT was not endotracheal as 230
Figure 1: Chest radiograph showing the endotracheal tube appearing to be endobronchial (right) but lying parallel to the tracheal shadow
detected by observation and auscultation. A direct laryngoscopic examination confirmed the ETT in the oesophagus which was promptly removed and airway secured with another ETT. Retrospectively, the chest radiograph taken in the emergency department [Figure 1] was examined. Initially, it appeared that the tip of the ETT was in the right main bronchus. A closer examination however revealed that the ETT was only partially overlapping the tracheal shadow and the ETT was actually lying parallel to the trachea and not inside it. Since trachea is a tubular structure, the margins of an ETT should always be within that of the trachea on a chest radiograph. An unsuspecting radiologist had reported the ETT to be right endobronchial! The lesson learnt here is that a chest radiograph can at times be confusing and the clinical methods to confirm the proper position of an ETT should never be neglected. A potential catastrophe was averted by the bedside standard five‑point auscultation and clinical judgement. The importance of clinical examination need not be overemphasised. If available, end‑tidal CO2 monitoring will be most useful to quickly confirm the endotracheal placement of the tube in doubtful cases. End‑tidal CO2 monitoring was not available in our intensive care unit.
Harihar V Hegde Department of Anaesthesiology, SDM College of Medical Sciences and Hospital, Sattur, Dharwad, Karnataka, India Address for correspondence: Dr. Harihar V Hegde, Department of Anaesthesiology, SDM College of Medical Sciences and Hospital, Sattur, Dharwad ‑ 580 009, Karnataka, India. E‑mail: [email protected]
Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
Copyright of Indian Journal of Anaesthesia is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
likely. The level of sensory block had also receded to T10 by that time. We therefore speculate that a centrally mediated decrease in sympathetic outflow and increase in parasympathetic outflow due to dexmedetomidine may be the cause. The patient’s autonomic response to peritoneal stretching could also be a contributing factor responsible for the severe bradycardia in this case. However, the bradycardia did not respond to the cessation of surgical handling and the usual dose of atropine. A fall in blood pressure and heart rate has been reported with various interventions like displacement of liver, insertion of hand into the peritoneal cavity, placement of packing and retraction of the wound edges. A vagally mediated reflex has been implicated in most cases, but exact pathways have not been established so far.[6] To conclude, although dexmedetomidine is an attractive intrathecal adjuvant for post-operative analgesia, we recommend meticulous use of this drug with vigilant monitoring in the operating room as well as in the post-anaesthesia care unit keeping in mind the possibility of delayed occurrence of severe bradycardia.
Tripat Kaur Bindra, Simarjot Singh Sarin1, Ruchi Gupta, Shubhdeep Departments of Anaesthesia and Critical Care and 1Cardiology, Sri Guru Ram Das Institute of Medical Sciences and Research, Sri Amritsar, Punjab, India Address for correspondence: Dr. Tripat Kaur Bindra, 4735A, Guru Nanak Wara, Amritsar, Punjab, India. E-mail: [email protected]
REFERENCES 1.
Al-Mustafa MM, Abu-Halaweh SA, Aloweidi AS, Murshidi MM, Ammari BA, Awwad ZM, et al. Effect of dexmedetomidine added to spinal bupivacaine for urological procedures. Saudi Med J 2009;30:365-70. 2. Bharati S, Pal A, Biswas C, Biswas R. Incidence of cardiac arrest increases with the indiscriminate use of dexmedetomidine: A case series and review of published case reports. Acta Anaesthesiol Taiwan 2011;49:165-7. 3. Ingersoll-Weng E, Manecke GR Jr, Thistlethwaite PA. Dexmedetomidine and cardiac arrest. Anesthesiology 2004;100:738-9. 4. Kanazi GE, Aouad MT, Jabbour-Khoury SI, Al Jazzar MD, Alameddine MM, Al-Yaman R, et al. Effect of low-dose dexmedetomidine or clonidine on the characteristics of bupivacaine spinal block. Acta Anaesthesiol Scand 2006;50:222-7. 5. Gupta R, Bogra J, Verma R, Kohli M, Kushwaha JK, Kumar S. Dexmedetomidine as an intrathecal adjuvant for postoperative analgesia. Indian J Anaesth 2011;55:347-51. 6. Doyle DJ, Mark PW. Reflex bradycardia during surgery. Can J Anaesth 1990;37:219-22. 228
Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.130851
Anaesthetic management of a case of distal myopathy Sir, Congenital myopathies are a group of rare genetic disorders characterized by a defect in the contractile apparatus of the myocytes.[1] We describe the case of a patient with distal myopathy taken up for total abdominal hysterectomy under general anesthesia as patient refused for neuraxial blockade. A 36‑years‑old female patient diagnosed to have abdominal leiomyosarcoma was planned for total abdominal hysterectomy under general anesthesia. On evaluation the patient gave a history of progressive weakness and thinning of distal aspect of both upper and lower limbs for the last 10 years. She had not sought any medical attention for these complaints. On examination, she was thin built with a BMI of 20. She was haemodynamically stable and had an adequate airway. She had atrophy of distal hand muscles with bilateral claw hands. She also had bilateral foot drop with a high stepping gait [Figure 1a and b]. Deep tendon reflexes, sensory nervous system, cranial nerves and spine examination were normal. Her routine investigations, chest X‑ray and ECG were normal. Electrophysiological studies were suggestive of distal myopathy with normal proximal muscles and sensory system.
a
b
Figure 1: Distal myopathy (with clawing of hand and foot drop) (a) Clawing of hand. (b) Foot drop Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
Letters to Editor
Tab. alprazolam 0.25 mg was given the night before the surgery and adequate blood products were arranged. In the operation theatre, before taking the patient in, all vapourizers were removed from anaesthesia workstation. Soda lime, breathing circuit and face mask were changed. After securing peripheral intravenous line and attaching standard monitors, we started intravenous induction with midazolam 1 mg, fentanyl 60 μcg and 1% propofol 60 mg. After loss of verbal response, we started neuromuscular monitoring with train of four (TOF) and gave atracurium 15 mg. After obtaining no response to TOF, airway was secured with proseal laryngeal mask airway (LMA) of size 3 and post induction monitoring included capnography, nasopharyngeal temperature and TOF count. Maintenance of anesthesia was with with O2/N2O and intravenous propofol infusion at 30-50 µcg/kg/min. Top up doses of atracurium was guided intraoperatively with the TOF count of 3 to achieve adequate muscle relaxation. Haemodynamics and respiratory parameters were maintained within the normal limits throughout the procedure. Thirty minutes before the end of the surgery, diclofenac 1.5 mg/kg and ondansetron 10 µcg/kg were given. At the end of the surgery, neuromuscular blockade was reversed with normal doses of neostigmine and glycopyrrolate and when TOF ratio was ≥0.9, proseal LMA was removed. Post operative period was uneventful. Anaesthetic management of patients with muscle diseases is challenging. In addition to unpredictable sporadic responses, such as rhabdomyolysis and metabolic stimulation, more predictable risks are associated with respiratory and bulbar muscle weakness, myocardial involvement, and difficult airway anatomy. To identify and minimize risk, a thorough preoperative workup is indispensable.[2,3] If regional anesthesia is planned, a preoperative assessment of peripheral sensory nerve dysfunction should be considered. Increased sensitivity to respiratory‑depressant drugs should be anticipated and where possible, doses should be titrated to the desired effect. Even with the most careful anaesthetic management, postoperative ventilatory support may be required and, therefore, postoperative intensive care unit availability should be planned. Baseline serum potassium and creatine kinase (CK) concentrations to assess muscle membrane integrity, family history, cardiac function test and other Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
syndromic features must be sought. It is possible that high baseline values may be associated with increased risk of profound perioperative rhabdomyolysis, whereas the baseline value per se is required to differentiate perioperative rhabdomyolysis from preexisting muscle damage.[3] All anesthetic techniques and drugs are associated with increased risk in patients with myopathies.[4,5] General anaesthesia performed as total intravenous anaesthesia or regional anaesthesia are equally safe. Inhalation agents especially halothane are not recommended because they may trigger a malignant hyperthermia (MH)‑like syndrome.[6] Consideration should be given to the use of short‑acting opioids to avoid the possibility of postoperative ventilation. Use of depolarizing neuromuscular blocking drugs should be generally discouraged in patients with neuromuscular diseases.[4,6] The depolarizing muscle relaxants might trigger MH, and prolonged depolarization leads to potassium release and calcium influx. Although theoretically reversal of neuromuscular block with anticholinesterases in patients with neuromuscular diseases may produce the similar situation, it was not observed in our case. So it can be recommended to use the normal dosage of reversal in such patients. The recent introduction of cyclodextrin reversal drugs (such as sugammadex) provides an attractive alternative in these circumstances. Succinylcholine may also cause acute profound rhabdomyolysis in patients susceptible to MH and those with myopathies. If neuromuscular blockade is required, a non‑depolarizing neuromuscular blocking drug should be used, keeping in mind that patients with myopathies may show increased sensitivity to these drugs. On the basis of cardiac evaluation, there may be an indication for invasive monitoring and use of inotropes in patients with identified cardiac involvement.[5] Strength and range of motion can deteriorate rapidly after surgery and immobilization, and anaesthesia can unmask subclinical respiratory failure.[7] So, patients should be mobilized as soon as possible after surgery.[8]
Neelam Agrawal, Ankur Sharma, Ravindra Batra Department of Anaesthesiology, All India Institute of Medical Sciences (AIIMS), New Delhi, India Address for correspondence: Dr. Ankur Sharma, C/O Mr. Suneel Vyas, C‑2/2287, Vasant Kunj, New Delhi, India. E‑mail: [email protected]
229
Letters to Editor
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8.
Cardamone M, Darras BT, Ryan MM. Inherited myopathies and muscular dystrophies. Semin Neurol 2008;28:250‑9. Nonaka I. Distal myopathies. Curr Opin Neurol 1999;12:493‑9. Klinger W, Rueffert H, Lehmann‑Horn F, Girard T, Hopkins PM. Core myopathies and risk of malignant hyperthermia. Anesth Analg 2009;109:1167‑73. Baraka AS, Jalbout MI. Anesthesia and Myopathy. Curr Opin Anesthesiol 2002;15:371‑6. Farag E, Barsoum S, Spagnuolo S, Tetzlaff J. Anesthesia and muscle disease. The Am J Anesthesiol 2000;27:491‑501. Jones R, Delacourt JL. Muscle rigidity following halothane anaesthesia in two patients with Freeman‑Sheldon Syndrome. Anaesthesiology 1992;77:599‑600. Ryan MM, Ilkovski B, Strickland CD, Schnell C, Sanoudou D, Midgett C, et al. Clinical course correlates poorly withmuscle pathology in nemaline myopathy. Neurology 2003;60:665‑73. Young HK, Lowe A, Fitzgerald DA, Seton C, Waters KA, Kenny E, et al. Non‑invasive ventilation in children with neuromuscular disease: A clinical and quality of life outcome study. Neurology 2007;68:198‑201. Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.130853
All endotracheal tubes that appear endotracheal are not so! Sir, We received a 30‑year‑old man into our intensive care unit who had met with a road traffic accident and suffered head injury. He was referred from another hospital after a resident there intubated him and transported on oxygen supplementation. On examination, the patient was in altered sensorium and agitated (Glasgow Coma Scale E4VTM5). The endotracheal tube (ETT) was fixed at 24 cm mark at the angle of the mouth. He was breathing spontaneously. There was equal movement and air entry on both sides of the chest with respiration. Oxygen saturation of haemoglobin could not be recorded before the administration of sedation as he was agitated. However, gurgling sounds were heard at the mouth. The ETT was connected to a T‑piece to administer oxygen and intravenous sedation was administered. Soon, there was oxygen desaturation even though breathing seemed adequate. An Ambu bag was used to ventilate the patient. It was evident immediately that the ETT was not endotracheal as 230
Figure 1: Chest radiograph showing the endotracheal tube appearing to be endobronchial (right) but lying parallel to the tracheal shadow
detected by observation and auscultation. A direct laryngoscopic examination confirmed the ETT in the oesophagus which was promptly removed and airway secured with another ETT. Retrospectively, the chest radiograph taken in the emergency department [Figure 1] was examined. Initially, it appeared that the tip of the ETT was in the right main bronchus. A closer examination however revealed that the ETT was only partially overlapping the tracheal shadow and the ETT was actually lying parallel to the trachea and not inside it. Since trachea is a tubular structure, the margins of an ETT should always be within that of the trachea on a chest radiograph. An unsuspecting radiologist had reported the ETT to be right endobronchial! The lesson learnt here is that a chest radiograph can at times be confusing and the clinical methods to confirm the proper position of an ETT should never be neglected. A potential catastrophe was averted by the bedside standard five‑point auscultation and clinical judgement. The importance of clinical examination need not be overemphasised. If available, end‑tidal CO2 monitoring will be most useful to quickly confirm the endotracheal placement of the tube in doubtful cases. End‑tidal CO2 monitoring was not available in our intensive care unit.
Harihar V Hegde Department of Anaesthesiology, SDM College of Medical Sciences and Hospital, Sattur, Dharwad, Karnataka, India Address for correspondence: Dr. Harihar V Hegde, Department of Anaesthesiology, SDM College of Medical Sciences and Hospital, Sattur, Dharwad ‑ 580 009, Karnataka, India. E‑mail: [email protected]
Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
Copyright of Indian Journal of Anaesthesia is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
