Letters to Editor
perfusion and no vascular sequelae. His limb mobility was preserved with good function. Ehlers‑Danlos syndrome is a disorder of connective tissue and can be classified into at least ten types on the basis of clinical, genetic and biochemical information.[1] The fragile skin and loose joints is often a result of abnormal genes that produce abnormal proteins which confer an inherited frailty of collagen. Among the different forms of Ehlers‑Danlos syndrome, type IV has a high incidence of vascular damage and is also known as vascular Ehlers‑Danlos syndrome, possibly present in the present case, though without the history of excessive bleeding or bruising. Patients with Ehlers‑Danlos syndrome type IV have been classically described to have four distinctive features:[1] characteristic faces (long thin nose and lips, sunken cheeks and bulging or protruding eyes), very thin and translucent skin, vascular fragility (tendency to bruise easily and rupture of vessels, especially the middle sized arteries) and rupture of viscera such as intestine and uterus.[2,3] Spontaneous rupture of arteries is the most common presenting symptom.[2] Most patients develop these complications before the age of 40. Median age in these patients is 48 years.[4] Cryptorchidism is frequently associated with connective tissue disorder as the guiding descending track is defective.[5] Venous fragility can cause excessive blood loss, hence adequate venous access, preferably elective central line should be ensured before induction. If regional anaesthesia is chosen, spinal anaesthesia has to be performed carefully to reduce chances of vascular trauma and it is possible that epidural anaesthesia also can lead to significant bleed in these cases. During general anaesthesia, there should be gentle laryngoscopy and intubation. Laxity of ligaments may increase chances of atlanto‑axial dislocations during forceful laryngoscopy. Laryngeal mask airway can cause increased pressures in pharyngeal areas, which can lead to soft‑tissue damage and vascular ooze.[6] The positioning of patients is important with emphasis on adequate padding of joints as skin trauma and also nerve palsies can occur. Careful and precise surgical technique with meticulous haemostasis and availability of a vascular surgeon is mandatory in these cases. High risk consent for vascular complications and subsequent critical care should be taken. Good venous access Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
before induction and extreme care during regional anaesthesia is important, especially avoiding epidural anaesthesia.
Kartik Syal, Dheeraj Singha, Ajay Sood Department of Anaesthesia, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India Address for correspondence: Dr. Kartik Syal, Department of Anaesthesia, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India. E‑mail: [email protected]
REFERENCES 1. Nerlich AG, Stöss H, Lehmann H, Krieg T, Müller PK. Pathomorphological and biochemical alterations in Ehlers‑Danlos‑syndrome type IV. Pathol Res Pract 1994;190:697‑706. 2. Germain DP, Herrera‑Guzman Y. Vascular Ehlers‑Danlos syndrome. Ann Genet 2004;47:1‑9. 3. Germain DP. Clinical and genetic features of vascular Ehlers‑Danlos syndrome. Ann Vasc Surg 2002;16:391‑7. 4. Pepin M, Schwarze U, Superti‑Furga A, Byers PH. Clinical and genetic features of Ehlers‑Danlos syndrome type IV, the vascular type. N Engl J Med 2000;342:673‑80. 5. Fallat M, Hersh J, HJ. Theories on the relationship between cryptorchidism and arthrogryposos. Pediatr Surg Int 1992;7:271‑3. 6. Liang MY, Hanko E, Dhamee MS. Ehlers‑Danlos syndrome type IV: Anesthetic considerations – Case report. Middle East J Anesthesiol 2006;18:1185‑9. Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.130846
Life‑threatening complication following infiltration with adrenaline Sir, An 8‑year‑old girl child of ASA PS Grade 1, weighing 22 kg, was posted for modified radical mastoidectomy for chronic otitis media. In the operating room, necessary monitoring and intravenous (IV) infusion of Ringer lactate was started. The induction was performed by an IV injection of propofol 40 mg, vecuronium 2 mg and fentanyl 30 µg, and endotracheal intubation was carried out after adequate muscle relaxation. Anaesthesia was 225
Letters to Editor
maintained with nitrous oxide (66 vol%) and isoflurane (1 vol%) in O2. The depth of anaesthesia was adequate as the vital parameters were stable and the patient was receiving approximately a total MAC of 1.4 of inhalational agents. After cleaning, painting and draping, the surgeon injected 60 µg of adrenaline (3 mL of 1:50,000 freshly prepared solution by diluting 1 mg of adrenaline in 49 mL of normal saline [NS]) subcutaneously at the incision site behind the pinna after negative aspiration over a period of 15-20 s. Within 30 s of the injection, the heart rate (HR) and blood pressure (BP) increased from 106 beats per minute (bpm) to 200-210 bpm and from 110/70 to 198/110 mmHg, respectively. The procedure was stopped and the patient was administered 100% O2. Within 2-3 min, the airway pressures rose to 18 cmH2O from 10 cmH2O with coarse crepitations and expiratory wheeze in all lung fields. There were no signs of airway obstruction. O2 saturation (SpO2) was 85-90% at FiO2 of 1. BP decreased to 75/40 mmHg with a HR of 160-165 bpm. Lead II in the electrocardiogram (ECG) showed sinus tachycardia. A provisional diagnosis of acute congestive heart failure was made. Inj. furosemide 5 mg IV and Inj. dobutamine at 7 µg/kg/min were administered. A urinary catheter was also inserted. Intermittent IV doses of Inj. vecuronium 0.4 mg and Inj. midazolam 0.4 mg were given. Tracheal suctioning revealed frothy secretions. Over a period of 1 h, the crepitations and wheeze gradually improved. BP could be now maintained at 100/65 mmHg without inotropes. Urine output was 100 mL. The SpO2 was 99% on FiO2 of 1. Arterial blood gas showed pH of 7.35, pCO2 of 45mmHg, pO2 152 mm Hg, BE ‑3mmol/l and bicarbonate of23mmmol/l. The trachea was extubated uneventfully after administration of reversal agent. After extubation, she was conscious and oriented. Her vitals were satisfactory (HR 140 bpm, BP 100/55 mmHg without any inotropes, respiratory rate 25/min) SpO2 was92% on air and 96% on venturi mask with FiO2 of 0.4. Auscultation showed few crepitations at the base of the lungs with normal heart sounds. The patient was shifted to the intensive care unit. Chest X‑ray, 12‑lead ECG, 2‑D ECHO and serum electrolytes were normal and she was discharged from the ICU after 2 days. Skin and subcutaneous tissue infiltration with adrenaline prior to incision is a common practice in an attempt to decrease the vascularity of the tissues, which improves the surgical field view and reduces the blood loss while operating on a vascular field like head and neck surgeries. The maximum recommended dose of adrenaline for infiltration is 5-10 µg/kg, which 226
may get altered due to simultaneous administration of inhaled anaesthetic agents.[1] It is noted that inhalational agents slow the automaticity of the sino‑atrial node and myocardial conduction, resulting in atrial and ventricular arrhythmias, which are further potentiated by the use of exogenous adrenaline.[2,3] Johnston et al. calculated the ED50 of adrenaline that produces arrhythmia with halothane to be 2.1 µg/kg and with isoflurane to be 6.7 µg/kg.[1] However, there are case reports suggesting the occurrence of severe hypertension, tachycardia, pulmonary oedema, life‑threatening arrhythmias and cardiac arrest on infiltration of only 20-30 µg of adrenaline.[4,5] Adding lignocaine to epinephrine has a protective action against cardiovascular complications as it stabilizes the myocardium by blocking sodium channels.[1,6] It is found that for subcutaneous infiltration, using 1:100,000 solution caused significant tachycardia than the 1:200,000 solution, and the 1:500,000 solution is virtually free of any side‑effects with a significant decrease in blood loss.[7,8] In our case, the surgeon slowly injected 60 µg of adrenaline for infiltration, which was well within the recommended doses. The cardiovascular crisis precipitated by the small dose was unexpected and dramatic. It could be due to accidental intravascular placement of the drug. Repeated aspirations while injecting are recommended. Using 1-2% lignocaine with adrenaline for infiltration is preferred as it has a protective action against arrhythmias, but, in our case, adrenaline was diluted in NS. Also, 1:50,000 adrenaline was used as compared with the standard recommended concentration of 1:100,000-1:200,000. Thus, it can be concluded that there are chances of severe cardiovascular crisis even after small recommended doses of adrenaline. Hence, one should be cautious while adrenaline is being injected.
Neha Gupta, Veena Gupta Department of Anaesthesia, Maharani Laxmi Bai Medical College, Jhansi, Uttar Pradesh, India Address for correspondence: Dr. Neha Gupta, H‑7, Veerangana Nagar, Kanpur Road, Jhansi ‑ 284 128, Uttar Pradesh, India. E‑mail: [email protected]
REFERENCES 1.
Johnston RR, Eger EI II, Wilson CA comparative interaction of epinephrine with enflurane, isoflurane, and halothane in man. Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
Letters to Editor Anesth Analg 1976;55:709‑12. Atlee JL 3rd, Bosjnak ZJ. Mechanisms for cardiac dysrhythmias during anesthesia. Anesthesiology 1990;72:347‑74. 3. Katz RL, Katz GJ. Surgical infiltration of pressor drugs and their interaction with volatile anaesthetics. Br J Anaesth 1966;38:712‑8. 4. Wanamaker HH, Arandia HY, Wanamaker HH. Epinephrine hypersensitivity‑induced cardiovascular crisis in otologic surgery. Otolaryngol Head Neck Surg 1994;111:841‑4. 5. Woldorf NM, Pastore PN. Extreme epinephrine sensitivity with a general anesthesia. Arch Otolaryngol 1972;96:272‑7. 6. Murthy HS, Rao GS. Cardiovascular responses to scalp infiltration with different concentrations of epinephrine with or without lidocaine during craniotomy. Anesth Analg 2001;92:1516‑9. 7. Hardwicke JT, Jordan RW, Skillman JM. Infiltration of epinephrine in reduction mammoplasty: A systematic review of the literature. Plast Reconstr Surg 2012;130:773‑8. 8. Thomas SS, Srivastava S, Nancarrow JD, Mohmand MH.Dilute adrenaline infiltration and reduced blood loss in reduction mammaplasty.Ann Plast Surg 1999;43:127‑31.
2.
Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.130850
Sinus arrest with intrathecal dexmedetomidine Sir, Dexmedetomidine, a highly selective α2 adrenoceptor agonist, is being increasingly used as an adjuvant in neuraxial blocks as it prolongs the sensory and motor block in a dose-dependent manner.[1] Severe bradycardia and cardiac arrest has been reported with the intravenous use of dexmedetomidine.[2,3] However, severe bradycardia progressing to sinus arrest after intrathecal administration of dexmedetomidine has not been reported. A 40-year-old female, 155 cm in height and weighing 65 kg, was scheduled for total abdominal hysterectomy. She had been operated for myomectomy under spinal anaesthesia 5 years back. Her general physical examination and all routine investigations were unremarkable. Upon arrival in the operating room, monitors were attached and her vitals were recorded. A peripheral venous access was established and preloaded with 500 mL of Ringer lactate. The subarachnoid space was reached in the L2-L3 interspace using a 25G Quincke’s needle with the patient in the left lateral Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
position. After ensuring free flow of cerebrospinal fluid, 2.5 mL of hyperbaric bupivacaine with 10 µg of dexmedetomidine was administered. The patient was positioned supine and oxygen was administered via a face mask at a rate of 5 L/min. The level of sensory block to pinprick was T10 after 2 min, and T6 was the highest level of sensory block achieved. The surgery commenced and the patient’s heart rate remained in the range of 50-60/min, with the blood pressure at around 130/80 mmHg. After about 70 min, when the surgeons were suturing the peritoneum, there was a sudden drop in her heart rate to 40/min. Immediately, the surgical handling was stopped and injection atropine 0.6 mg was given intravenously, to which there was no response for 3 min. Meanwhile, she complained of some discomfort in her epigastrium and her heart rate further dropped to 34/min while her blood pressure was 124/76 mmHg with SpO2 of 99%. Another dose of inj. atropine 0.6 mg was given intravenously but her heart rate dropped to 18/min over 5 s followed by sinus arrest. Then, the third dose of inj. atropine 0.6 mg was given, which led to an increase in her heart rate to 86/min. The level of sensory blockade was T10 at this time and the SpO2 was consistently 99%. The surgery was completed in the next 15 min uneventfully and the estimated blood loss was around 200 mL. The patient remained comfortable with a heart rate of around 74/min and blood pressure of 124/86 mmHg. Her post-operative Holter monitoring and echocardiography were unremarkable. Intrathecal dexmedetomidine when combined with spinal bupivacaine produces earlier onset and prolonged duration of sensory and motor block with excellent quality of post-operative analgesia without significant haemodynamic alterations.[1,4] Although episodes of sinus arrest and severe bradycardia progressing to asystole have been reported in patients receiving intravenous dexmedetomidine,[2,3] no severe cardiovascular complications have been observed with intrathecal dexmedetomidine. Two cases of bradycardia (heart rate 50/min) have been observed by Gupta et al. when they used 5 µg of dexmedetomidine as an intrathecal adjuvant for post-operative analgesia.[5] The two very unusual features observed in our case were the time to the occurrence of sinus arrest and the high dose of atropine required for its treatment. As 1 h had elapsed between the intrathecal administration of drugs and the sinus arrest, sinus arrest due to sympathetic blockade due to bupivacaine was less 227
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.
perfusion and no vascular sequelae. His limb mobility was preserved with good function. Ehlers‑Danlos syndrome is a disorder of connective tissue and can be classified into at least ten types on the basis of clinical, genetic and biochemical information.[1] The fragile skin and loose joints is often a result of abnormal genes that produce abnormal proteins which confer an inherited frailty of collagen. Among the different forms of Ehlers‑Danlos syndrome, type IV has a high incidence of vascular damage and is also known as vascular Ehlers‑Danlos syndrome, possibly present in the present case, though without the history of excessive bleeding or bruising. Patients with Ehlers‑Danlos syndrome type IV have been classically described to have four distinctive features:[1] characteristic faces (long thin nose and lips, sunken cheeks and bulging or protruding eyes), very thin and translucent skin, vascular fragility (tendency to bruise easily and rupture of vessels, especially the middle sized arteries) and rupture of viscera such as intestine and uterus.[2,3] Spontaneous rupture of arteries is the most common presenting symptom.[2] Most patients develop these complications before the age of 40. Median age in these patients is 48 years.[4] Cryptorchidism is frequently associated with connective tissue disorder as the guiding descending track is defective.[5] Venous fragility can cause excessive blood loss, hence adequate venous access, preferably elective central line should be ensured before induction. If regional anaesthesia is chosen, spinal anaesthesia has to be performed carefully to reduce chances of vascular trauma and it is possible that epidural anaesthesia also can lead to significant bleed in these cases. During general anaesthesia, there should be gentle laryngoscopy and intubation. Laxity of ligaments may increase chances of atlanto‑axial dislocations during forceful laryngoscopy. Laryngeal mask airway can cause increased pressures in pharyngeal areas, which can lead to soft‑tissue damage and vascular ooze.[6] The positioning of patients is important with emphasis on adequate padding of joints as skin trauma and also nerve palsies can occur. Careful and precise surgical technique with meticulous haemostasis and availability of a vascular surgeon is mandatory in these cases. High risk consent for vascular complications and subsequent critical care should be taken. Good venous access Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
before induction and extreme care during regional anaesthesia is important, especially avoiding epidural anaesthesia.
Kartik Syal, Dheeraj Singha, Ajay Sood Department of Anaesthesia, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India Address for correspondence: Dr. Kartik Syal, Department of Anaesthesia, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India. E‑mail: [email protected]
REFERENCES 1. Nerlich AG, Stöss H, Lehmann H, Krieg T, Müller PK. Pathomorphological and biochemical alterations in Ehlers‑Danlos‑syndrome type IV. Pathol Res Pract 1994;190:697‑706. 2. Germain DP, Herrera‑Guzman Y. Vascular Ehlers‑Danlos syndrome. Ann Genet 2004;47:1‑9. 3. Germain DP. Clinical and genetic features of vascular Ehlers‑Danlos syndrome. Ann Vasc Surg 2002;16:391‑7. 4. Pepin M, Schwarze U, Superti‑Furga A, Byers PH. Clinical and genetic features of Ehlers‑Danlos syndrome type IV, the vascular type. N Engl J Med 2000;342:673‑80. 5. Fallat M, Hersh J, HJ. Theories on the relationship between cryptorchidism and arthrogryposos. Pediatr Surg Int 1992;7:271‑3. 6. Liang MY, Hanko E, Dhamee MS. Ehlers‑Danlos syndrome type IV: Anesthetic considerations – Case report. Middle East J Anesthesiol 2006;18:1185‑9. Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.130846
Life‑threatening complication following infiltration with adrenaline Sir, An 8‑year‑old girl child of ASA PS Grade 1, weighing 22 kg, was posted for modified radical mastoidectomy for chronic otitis media. In the operating room, necessary monitoring and intravenous (IV) infusion of Ringer lactate was started. The induction was performed by an IV injection of propofol 40 mg, vecuronium 2 mg and fentanyl 30 µg, and endotracheal intubation was carried out after adequate muscle relaxation. Anaesthesia was 225
Letters to Editor
maintained with nitrous oxide (66 vol%) and isoflurane (1 vol%) in O2. The depth of anaesthesia was adequate as the vital parameters were stable and the patient was receiving approximately a total MAC of 1.4 of inhalational agents. After cleaning, painting and draping, the surgeon injected 60 µg of adrenaline (3 mL of 1:50,000 freshly prepared solution by diluting 1 mg of adrenaline in 49 mL of normal saline [NS]) subcutaneously at the incision site behind the pinna after negative aspiration over a period of 15-20 s. Within 30 s of the injection, the heart rate (HR) and blood pressure (BP) increased from 106 beats per minute (bpm) to 200-210 bpm and from 110/70 to 198/110 mmHg, respectively. The procedure was stopped and the patient was administered 100% O2. Within 2-3 min, the airway pressures rose to 18 cmH2O from 10 cmH2O with coarse crepitations and expiratory wheeze in all lung fields. There were no signs of airway obstruction. O2 saturation (SpO2) was 85-90% at FiO2 of 1. BP decreased to 75/40 mmHg with a HR of 160-165 bpm. Lead II in the electrocardiogram (ECG) showed sinus tachycardia. A provisional diagnosis of acute congestive heart failure was made. Inj. furosemide 5 mg IV and Inj. dobutamine at 7 µg/kg/min were administered. A urinary catheter was also inserted. Intermittent IV doses of Inj. vecuronium 0.4 mg and Inj. midazolam 0.4 mg were given. Tracheal suctioning revealed frothy secretions. Over a period of 1 h, the crepitations and wheeze gradually improved. BP could be now maintained at 100/65 mmHg without inotropes. Urine output was 100 mL. The SpO2 was 99% on FiO2 of 1. Arterial blood gas showed pH of 7.35, pCO2 of 45mmHg, pO2 152 mm Hg, BE ‑3mmol/l and bicarbonate of23mmmol/l. The trachea was extubated uneventfully after administration of reversal agent. After extubation, she was conscious and oriented. Her vitals were satisfactory (HR 140 bpm, BP 100/55 mmHg without any inotropes, respiratory rate 25/min) SpO2 was92% on air and 96% on venturi mask with FiO2 of 0.4. Auscultation showed few crepitations at the base of the lungs with normal heart sounds. The patient was shifted to the intensive care unit. Chest X‑ray, 12‑lead ECG, 2‑D ECHO and serum electrolytes were normal and she was discharged from the ICU after 2 days. Skin and subcutaneous tissue infiltration with adrenaline prior to incision is a common practice in an attempt to decrease the vascularity of the tissues, which improves the surgical field view and reduces the blood loss while operating on a vascular field like head and neck surgeries. The maximum recommended dose of adrenaline for infiltration is 5-10 µg/kg, which 226
may get altered due to simultaneous administration of inhaled anaesthetic agents.[1] It is noted that inhalational agents slow the automaticity of the sino‑atrial node and myocardial conduction, resulting in atrial and ventricular arrhythmias, which are further potentiated by the use of exogenous adrenaline.[2,3] Johnston et al. calculated the ED50 of adrenaline that produces arrhythmia with halothane to be 2.1 µg/kg and with isoflurane to be 6.7 µg/kg.[1] However, there are case reports suggesting the occurrence of severe hypertension, tachycardia, pulmonary oedema, life‑threatening arrhythmias and cardiac arrest on infiltration of only 20-30 µg of adrenaline.[4,5] Adding lignocaine to epinephrine has a protective action against cardiovascular complications as it stabilizes the myocardium by blocking sodium channels.[1,6] It is found that for subcutaneous infiltration, using 1:100,000 solution caused significant tachycardia than the 1:200,000 solution, and the 1:500,000 solution is virtually free of any side‑effects with a significant decrease in blood loss.[7,8] In our case, the surgeon slowly injected 60 µg of adrenaline for infiltration, which was well within the recommended doses. The cardiovascular crisis precipitated by the small dose was unexpected and dramatic. It could be due to accidental intravascular placement of the drug. Repeated aspirations while injecting are recommended. Using 1-2% lignocaine with adrenaline for infiltration is preferred as it has a protective action against arrhythmias, but, in our case, adrenaline was diluted in NS. Also, 1:50,000 adrenaline was used as compared with the standard recommended concentration of 1:100,000-1:200,000. Thus, it can be concluded that there are chances of severe cardiovascular crisis even after small recommended doses of adrenaline. Hence, one should be cautious while adrenaline is being injected.
Neha Gupta, Veena Gupta Department of Anaesthesia, Maharani Laxmi Bai Medical College, Jhansi, Uttar Pradesh, India Address for correspondence: Dr. Neha Gupta, H‑7, Veerangana Nagar, Kanpur Road, Jhansi ‑ 284 128, Uttar Pradesh, India. E‑mail: [email protected]
REFERENCES 1.
Johnston RR, Eger EI II, Wilson CA comparative interaction of epinephrine with enflurane, isoflurane, and halothane in man. Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
Letters to Editor Anesth Analg 1976;55:709‑12. Atlee JL 3rd, Bosjnak ZJ. Mechanisms for cardiac dysrhythmias during anesthesia. Anesthesiology 1990;72:347‑74. 3. Katz RL, Katz GJ. Surgical infiltration of pressor drugs and their interaction with volatile anaesthetics. Br J Anaesth 1966;38:712‑8. 4. Wanamaker HH, Arandia HY, Wanamaker HH. Epinephrine hypersensitivity‑induced cardiovascular crisis in otologic surgery. Otolaryngol Head Neck Surg 1994;111:841‑4. 5. Woldorf NM, Pastore PN. Extreme epinephrine sensitivity with a general anesthesia. Arch Otolaryngol 1972;96:272‑7. 6. Murthy HS, Rao GS. Cardiovascular responses to scalp infiltration with different concentrations of epinephrine with or without lidocaine during craniotomy. Anesth Analg 2001;92:1516‑9. 7. Hardwicke JT, Jordan RW, Skillman JM. Infiltration of epinephrine in reduction mammoplasty: A systematic review of the literature. Plast Reconstr Surg 2012;130:773‑8. 8. Thomas SS, Srivastava S, Nancarrow JD, Mohmand MH.Dilute adrenaline infiltration and reduced blood loss in reduction mammaplasty.Ann Plast Surg 1999;43:127‑31.
2.
Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.130850
Sinus arrest with intrathecal dexmedetomidine Sir, Dexmedetomidine, a highly selective α2 adrenoceptor agonist, is being increasingly used as an adjuvant in neuraxial blocks as it prolongs the sensory and motor block in a dose-dependent manner.[1] Severe bradycardia and cardiac arrest has been reported with the intravenous use of dexmedetomidine.[2,3] However, severe bradycardia progressing to sinus arrest after intrathecal administration of dexmedetomidine has not been reported. A 40-year-old female, 155 cm in height and weighing 65 kg, was scheduled for total abdominal hysterectomy. She had been operated for myomectomy under spinal anaesthesia 5 years back. Her general physical examination and all routine investigations were unremarkable. Upon arrival in the operating room, monitors were attached and her vitals were recorded. A peripheral venous access was established and preloaded with 500 mL of Ringer lactate. The subarachnoid space was reached in the L2-L3 interspace using a 25G Quincke’s needle with the patient in the left lateral Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
position. After ensuring free flow of cerebrospinal fluid, 2.5 mL of hyperbaric bupivacaine with 10 µg of dexmedetomidine was administered. The patient was positioned supine and oxygen was administered via a face mask at a rate of 5 L/min. The level of sensory block to pinprick was T10 after 2 min, and T6 was the highest level of sensory block achieved. The surgery commenced and the patient’s heart rate remained in the range of 50-60/min, with the blood pressure at around 130/80 mmHg. After about 70 min, when the surgeons were suturing the peritoneum, there was a sudden drop in her heart rate to 40/min. Immediately, the surgical handling was stopped and injection atropine 0.6 mg was given intravenously, to which there was no response for 3 min. Meanwhile, she complained of some discomfort in her epigastrium and her heart rate further dropped to 34/min while her blood pressure was 124/76 mmHg with SpO2 of 99%. Another dose of inj. atropine 0.6 mg was given intravenously but her heart rate dropped to 18/min over 5 s followed by sinus arrest. Then, the third dose of inj. atropine 0.6 mg was given, which led to an increase in her heart rate to 86/min. The level of sensory blockade was T10 at this time and the SpO2 was consistently 99%. The surgery was completed in the next 15 min uneventfully and the estimated blood loss was around 200 mL. The patient remained comfortable with a heart rate of around 74/min and blood pressure of 124/86 mmHg. Her post-operative Holter monitoring and echocardiography were unremarkable. Intrathecal dexmedetomidine when combined with spinal bupivacaine produces earlier onset and prolonged duration of sensory and motor block with excellent quality of post-operative analgesia without significant haemodynamic alterations.[1,4] Although episodes of sinus arrest and severe bradycardia progressing to asystole have been reported in patients receiving intravenous dexmedetomidine,[2,3] no severe cardiovascular complications have been observed with intrathecal dexmedetomidine. Two cases of bradycardia (heart rate 50/min) have been observed by Gupta et al. when they used 5 µg of dexmedetomidine as an intrathecal adjuvant for post-operative analgesia.[5] The two very unusual features observed in our case were the time to the occurrence of sinus arrest and the high dose of atropine required for its treatment. As 1 h had elapsed between the intrathecal administration of drugs and the sinus arrest, sinus arrest due to sympathetic blockade due to bupivacaine was less 227
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.
