Letters to Editor
The technique of CSEA with low dose intrathecal hyperbaric bupivacaine and EVE provided rapid onset with profound surgical anaesthesia due to spinal and ability to prolong the blockade by epidural. Administration of low dose spinal with opioid and EVE not only provided adequate level of block but also provided stable haemodynamics in the peri‑operative period. Various authors[3,4] have utilised the technique of EVE to achieve the desired effect, without significant haemodynamic effect and faster recovery of motor function. A study by Blumgart et al.[5] suggested a higher level of analgesia with EVE compared with spinal alone. This is secondary to the volume effect in epidural space which compresses the subarachnoid space and increase the intrathecal spread of the drug. Goy[6] demonstrated that the mean effective dose of intrathecal hyperbaric bupivacaine in CSE was 20% less than that in single shot spinal. Our result was similar to reports of use of the technique in pregnant females with peripartum cardiomyopathy.[7] CSE with EVE technique has been used for gynaecological and orthopaedic surgery, but this is probably the first report of its use in renal transplantation in uremic cardiomyopathy.
A prospective, randomized, double‑blind study. Anesth Analg 2004;98:810‑4. 5. Blumgart CH, Ryall D, Dennison B, Thompson‑Hill LM. Mechanism of extension of spinal anaesthesia by extradural injection of local anaesthetic. Br J Anaesth 1992;69:457‑60. 6. Goy RW, Chee‑Seng Y, Sia AT, Choo‑Kok K, Liang S. The median effective dose of intrathecal hyperbaric bupivacaine is larger in the single‑shot spinal as compared with the combined spinal‑epidural technique. Anesth Analg 2005;100:1499‑502. 7. Toda N, Maeda K, Shoji E, Suzuki T, Kitaura M, Nishimoto M. Combined spinal‑epidural anesthesia for cesarean section in a patient with dilated cardiomyopathy. Masui 2008;57:187‑90. Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.126845
Myocardial infarction during pregnancy: A rare occurrence Sir,
Patients who have uremic cardiomyopathy and poor LV function are high risk for general anaesthesia, low dose spinal with EVE may be used as an option for providing safe intra‑operative anaesthesia and prolong post‑operative analgesia.
Vinit K Srivastava, Sanjay Agrawal1, Praveen K Das2, Mukadder Ahmed3 Department of Anaesthesia, 3Apollo Hospitals, Bilaspur, Chhattisgarh, 1 Himalayan Institute of Medical Sciences, Dehradun, Uttarakhand, 2 Dr. RML Institute of Medical Sciences, Lucknow, Uttar Pradesh, India Address for correspondence: Dr. Vinit K Srivastava, Department of Anaesthesia, Apollo Hospitals, Bilaspur ‑ 495 006, Chhattisgarh, India. E‑mail: [email protected]
REFERENCES 1.
Vanholder R, Glorieux G, Lameire N, European Uremic Toxin Work Group. Uraemic toxins and cardiovascular disease. Nephrol Dial Transplant 2003;18:463‑6. 2. Nicholls AJ, Tucker V, Gibbs P. Awake renal transplantation; a realistic alternative to general anesthesia. Transplant Proc 2010;42:1677‑8. 3. Loubert C, O’Brien PJ, Fernando R, Walton N, Philip S, Addei T, et al. Epidural volume extension in combined spinal epidural anaesthesia for elective caesarean section: A randomised controlled trial. Anaesthesia 2011;66:341‑7. 4. Lew E, Yeo SW, Thomas E. Combined spinal‑epidural anesthesia using epidural volume extension leads to faster motor recovery after elective cesarean delivery: 94
Pregnancy‑associated acute myocardial infarction (AMI) is rare, but is associated with high morbidity and mortality. The estimated incidence of AMI during pregnancy is 3‑10 cases/100,000 deliveries with a maternal mortality rate of 21% and fetal mortality rate of 13%.[1] Pregnancy‑associated changes in the cardiovascular system and coagulation system increases the risk of AMI by approximately 3 to 4‑fold.[1] We describe a case of AMI and its management during caesarean delivery in our institute. A 30‑year‑old female, gravida 5, para 4, at 36 weeks of gestation got admitted with the complaints of bleeding per vagina and diffuse abdominal pain. Patient was in distress, but alert and oriented. Her pulse was 140/min and blood pressure (BP) was 74/46 mm Hg. After securing two peripheral lines, initial intravenous fluids resuscitation was carried out by administrating 1500 ml crystalloid (lactated ringer solution) and 500 ml colloid (hydroxyethyl starch 130/0.4). As the BP was very low dopamine infusion at 12 mcg/kg/min was started simultaneously. Over a period of time as haemodynamics improved and patient started responding to fluid therapy; dopamine infusion was titrated according to BP. On auscultation of chest normal vesicular breath sounds were heard. The Indian Journal of Anaesthesia | Vol. 58| Issue 1 | Jan-Feb 2014
Letters to Editor
cardiac examination revealed no obvious murmurs, gallops or pericardial rub. The electrocardiogram (ECG) demonstrated normal sinus rhythm with ST segment T wave changes in all leads, which was attributed to tachycardia, hypotension and anaemia. Laboratory results were as follows: Haemoglobin ‑ 5.5 g/dl, haematocrit ‑ 17.6%, total leukocyte count ‑ 14,500/ul, platelet count ‑.2.44 lac/ul, Random Blood Sugar (RBS) ‑ 79 mg/dl, blood urea nitrogen ‑ 23 mg/dl, S.creatinine ‑ 0.79 mg/dl, S.bilirubin ‑ 0.93 mg/dl, serum glutamic oxaloacetic transaminase/serum glutamic pyruvic transaminase ‑ 36/39 IU/L and S.alkaline phosphatase ‑ 369 IU/L. Ultrasonography revealed single intrauterine live foetus of gestational age 34.5 weeks with placenta previa grade 3. Patient received two units of packed red blood cells. Her BP picked up to 106/54 mm Hg on dopamine infusion (7 mcg/kg/min) and was posted for emergency caesarean section. General anaesthesia was planned due to haemodynamic instability of the patient. Rapid sequence induction was performed using propofol 1 mg/kg and ketamine 1 mg/kg and concomitant preoxygenation. Endotracheal intubation was done following injection of succinylcholine 1.5 mg/kg. Patient was maintained on isoflurane 0.7% with O2/N2O (40/60) and atracurium 0.5 mg/kg. Just after delivery of baby, patient developed pulseless ventricular tachycardia. Cardiopulmonary resuscitation was started immediately. Meanwhile, defibrillator was prepared and a shock of 150 joule (biphasic waveform) was delivered. Patient reverted to sinus rhythm, but ST segment elevation appeared on continuous ECG monitoring. Injection oxytocin 10 units was added to 1 L of ringer lactate and given at a rate of 10 ml/min. Patient remained stable during the rest of surgery and was shifted to intensive care unit for elective ventilation and further management. A 12 lead ECG in the immediate post‑operative period showed normal sinus rhythm with ST segment elevation and T wave inversion in lead I, aVL and V1 to V4. Laboratory results were as follows: Troponin I positive; creatinine kinase‑MB fraction ‑ 39 U/L; triglycerides ‑ 310 mg/dL; total cholesterol ‑ 250 mg/dL;high‑density‑lipoprotein‑38 mg/dL and low‑density‑lipoprotein ‑ 163 mg/dL. Cardiologist consultation and bedside echocardiography demonstrated left ventricular wall motion abnormalities at the apex and anterior wall; and ejection fraction of 35 to 40% and mild mitral regurgitation. Patient was treated with aspirin, clopidogrel, unfractionated heparin, Indian Journal of Anaesthesia | Vol. 58| Issue 1 | Jan-Feb 2014
metoprolol and morphine. In the next 24 h patient was weaned off from the ventilator and vasopressor support and was shifted to cardiac catheterization laboratory, where angiography revealed 80% block of left anterior descending artery, but no active intervention was done at that time. Patient was transferred to the cardiac intensive care unit (CICU) and started on a regimen of carvedilol, 12.5 mg; aspirin, 150 mg; clopidogrel, 75 mg; atorvastatin, 20 mg and ivabradine, 7.5 mg. Patient remained stable in CICU and on day 3 she was transferred back to the ward and was discharged on the 7th day with the advice of cardiology follow‑up. The most common underlying mechanisms implicated in AMI during pregnancy are atherosclerotic coronary artery disease (CAD), coronary thrombosis with hypercoagulability and coronary artery dissection. Complications of pregnancy that are significantly associated with AMI are severe anaemia, preeclampsia, postpartum haemorrhage, postpartum infection, shock, ergometrine, prostaglandin E1, fluid and electrolyte imbalances.[2‑5] All causes of tachycardia, hypertension, hypotension, anaemia and pain should be treated aggressively. The interventions include vasopressors to maintain BP, β‑blockers to slow heart rate, managing blood volume, post‑operative pain and respiratory function. Emergent coronary intervention, anticoagulants or glycoprotein IIb/IIIa antagonists are rarely indicated in the immediate post‑operative course and are hazardous because of the risk of bleeding, unless ST elevation or intractable cardiogenic shock ensues.[6] With this case report, we highlight the possibility of presence of unknown CAD and occurrence of perioperative AMI, apart from tachycardia and anaemia in pregnant patients having ST‑T changes in ECG. Tachycardia, hypotension, hypertension, anaemia, hypoxemia and systolic and diastolic myocardial dysfunction are common causes of prolonged ST‑depression and myocardial infarction in patients with stable CAD undergoing major noncardiac surgery. Careful perioperative monitoring for ischemia, a low threshold for treating and preventing tachycardia while avoiding hypotension, decreased cardiac output and/or cardiac decompensation help prevent perioperative myocardial infarction (PMI). Coronary intervention is rarely indicated as the first line of treatment and antithrombotic therapy may exacerbate bleeding. Future studies are needed to determine, which patients with PMI require intensified post‑operative surveillance, 95
Letters to Editor
medical therapy and/or coronary intervention to improve the long‑term survival.
Sadik Mohammed, Rakesh Karnawat, PK Bhatia1, Ghansham Biyani2 Departments of Anaesthesiology, Dr. S. N. Medical College, 1AIIMS, Jodhpur, Rajasthan, 2Department of Anaesthesiology, AIIMS, New Delhi, India Address for correspondence: Dr. Sadik Mohammed, Near Mohammedi Masjid, Hanuman Ji Ki Bhakhari, Nai Sarak, Jodhpur ‑ 342 001, Rajasthan, India. E‑mail: [email protected]
ReferenceS 1.
Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. Ann Intern Med 1996;125:751‑62. 2. James AH, Jamison MG, Biswas MS, Brancazio LR, Swamy GK, Myers ER. Acute myocardial infarction in pregnancy: A United States population‑based study. Circulation 2006;113:1564‑71. 3. Poh CL, Lee CH. Acute myocardial infarction in pregnant women. Ann Acad Med Singapore 2010;39:247‑53. 4. Sutaria N, O'Toole L, Northridge D. Postpartum acute MI following routine ergometrine administration treated successfully by primary PTCA. Heart 2000;83:97‑8. 5. Schulte‑Sasse U. Life threatening myocardial ischaemia associated with the use of prostaglandin E1 to induce abortion. BJOG 2000;107:700‑2. 6. Berger PB, Bellot V, Bell MR, Horlocker TT, Rihal CS, Hallett JW, et al. An immediate invasive strategy for the treatment of acute myocardial infarction early after noncardiac surgery. Am J Cardiol 2001;87:1100‑2, A6, A9. Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.126846
Dexmedetomidine in the management of severe tetanus Sir, Although tetanus is a rare disease in the developed countries now, it remains a significant cause of death world-wide and is associated with a high rate of mortality. Components of severe tetanus management are supportive care with sedation, airway protection and controlled ventilation.[1] Dexmedetomidine is a high selective α-2-receptor agonist. It has combined analgesic and anti-sympathetic effect without respiratory system depression. There have been several studies describing its successful use in 96
mechanically ventilated patients for short- (24 h) and long-term (up to 7 days) use in the intensive care unit (ICU).[2] Dexmedetomidine has been also used in the treatment of tetanus in six patients for 7 days.[3] We present a case of generalised tetanus complicated by uncontrolled sympathetic over activity (SOA) managed with dexmedetomidine infusion. A 53-year-old male patient presented with complaints of dyspnoea, upper lip twitching, difficulty in swallowing and a local abscess around his right foot. He had a medical history of penetrating wound in his right foot 11 days before. Antibiotics and human tetanus immunoglobulin were administered and the wound was surgically debrided. Because of respiratory failure with SOA, he was intubated and mechanically ventilated. SOA persisted despite midazolam and magnesium sulphate infusion. Dexmedetomidine infusion was started on day 5 and SOA could be controlled successfully. On day 10, severe bronchopneumonia developed and the patient died on day 12. The management of tetanus requires the prevention of tetanospasmin absorption, treatment of symptoms, stabilisation of autonomic instability, antibiotic therapy and control of the airway with assisted ventilation if indicated. Basal SOA is characterised by resting tachycardia and depression of bowel motility and bladder function, while severe SOA presents with fluctuating tachycardia, labile hypertension and sweating with and without stimulation.[4] Different methods to control SOA have been provided, including magnesium sulphate infusions, dantrolene infusions, intrathecal administration of baclofen, benzodiazepine, clonidine and dexmedetomidine.[5] Girgin et al.[3] reported use of dexmedetomidine in the management of tetanus for 7 days in six patients without any side-effects. According to the same author, its administration did not fully control the muscle spasm, but decreased their frequency and severity and reduced the use of sedative drugs to control muscle spasms and cardiovascular instability. In this case, we started dexmedetomidine infusion on the 5th day in the ICU, because midazolam and magnesium sulphate infusions did not efficiently control SOA. We observed that tachycardia (heart rate >110 beats/ min) and hypertension (mean arterial blood pressure >100 mmHg) decreased to acceptable normal levels and need for sedative drugs was reduced after starting dexmedetomidine infusion. However, we were not able to fully avoid their use. We used dexmedetomidine for 4 days. Although hypotension and bradycardia are the Indian Journal of Anaesthesia | Vol. 58| Issue 1 | Jan-Feb 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.
The technique of CSEA with low dose intrathecal hyperbaric bupivacaine and EVE provided rapid onset with profound surgical anaesthesia due to spinal and ability to prolong the blockade by epidural. Administration of low dose spinal with opioid and EVE not only provided adequate level of block but also provided stable haemodynamics in the peri‑operative period. Various authors[3,4] have utilised the technique of EVE to achieve the desired effect, without significant haemodynamic effect and faster recovery of motor function. A study by Blumgart et al.[5] suggested a higher level of analgesia with EVE compared with spinal alone. This is secondary to the volume effect in epidural space which compresses the subarachnoid space and increase the intrathecal spread of the drug. Goy[6] demonstrated that the mean effective dose of intrathecal hyperbaric bupivacaine in CSE was 20% less than that in single shot spinal. Our result was similar to reports of use of the technique in pregnant females with peripartum cardiomyopathy.[7] CSE with EVE technique has been used for gynaecological and orthopaedic surgery, but this is probably the first report of its use in renal transplantation in uremic cardiomyopathy.
A prospective, randomized, double‑blind study. Anesth Analg 2004;98:810‑4. 5. Blumgart CH, Ryall D, Dennison B, Thompson‑Hill LM. Mechanism of extension of spinal anaesthesia by extradural injection of local anaesthetic. Br J Anaesth 1992;69:457‑60. 6. Goy RW, Chee‑Seng Y, Sia AT, Choo‑Kok K, Liang S. The median effective dose of intrathecal hyperbaric bupivacaine is larger in the single‑shot spinal as compared with the combined spinal‑epidural technique. Anesth Analg 2005;100:1499‑502. 7. Toda N, Maeda K, Shoji E, Suzuki T, Kitaura M, Nishimoto M. Combined spinal‑epidural anesthesia for cesarean section in a patient with dilated cardiomyopathy. Masui 2008;57:187‑90. Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.126845
Myocardial infarction during pregnancy: A rare occurrence Sir,
Patients who have uremic cardiomyopathy and poor LV function are high risk for general anaesthesia, low dose spinal with EVE may be used as an option for providing safe intra‑operative anaesthesia and prolong post‑operative analgesia.
Vinit K Srivastava, Sanjay Agrawal1, Praveen K Das2, Mukadder Ahmed3 Department of Anaesthesia, 3Apollo Hospitals, Bilaspur, Chhattisgarh, 1 Himalayan Institute of Medical Sciences, Dehradun, Uttarakhand, 2 Dr. RML Institute of Medical Sciences, Lucknow, Uttar Pradesh, India Address for correspondence: Dr. Vinit K Srivastava, Department of Anaesthesia, Apollo Hospitals, Bilaspur ‑ 495 006, Chhattisgarh, India. E‑mail: [email protected]
REFERENCES 1.
Vanholder R, Glorieux G, Lameire N, European Uremic Toxin Work Group. Uraemic toxins and cardiovascular disease. Nephrol Dial Transplant 2003;18:463‑6. 2. Nicholls AJ, Tucker V, Gibbs P. Awake renal transplantation; a realistic alternative to general anesthesia. Transplant Proc 2010;42:1677‑8. 3. Loubert C, O’Brien PJ, Fernando R, Walton N, Philip S, Addei T, et al. Epidural volume extension in combined spinal epidural anaesthesia for elective caesarean section: A randomised controlled trial. Anaesthesia 2011;66:341‑7. 4. Lew E, Yeo SW, Thomas E. Combined spinal‑epidural anesthesia using epidural volume extension leads to faster motor recovery after elective cesarean delivery: 94
Pregnancy‑associated acute myocardial infarction (AMI) is rare, but is associated with high morbidity and mortality. The estimated incidence of AMI during pregnancy is 3‑10 cases/100,000 deliveries with a maternal mortality rate of 21% and fetal mortality rate of 13%.[1] Pregnancy‑associated changes in the cardiovascular system and coagulation system increases the risk of AMI by approximately 3 to 4‑fold.[1] We describe a case of AMI and its management during caesarean delivery in our institute. A 30‑year‑old female, gravida 5, para 4, at 36 weeks of gestation got admitted with the complaints of bleeding per vagina and diffuse abdominal pain. Patient was in distress, but alert and oriented. Her pulse was 140/min and blood pressure (BP) was 74/46 mm Hg. After securing two peripheral lines, initial intravenous fluids resuscitation was carried out by administrating 1500 ml crystalloid (lactated ringer solution) and 500 ml colloid (hydroxyethyl starch 130/0.4). As the BP was very low dopamine infusion at 12 mcg/kg/min was started simultaneously. Over a period of time as haemodynamics improved and patient started responding to fluid therapy; dopamine infusion was titrated according to BP. On auscultation of chest normal vesicular breath sounds were heard. The Indian Journal of Anaesthesia | Vol. 58| Issue 1 | Jan-Feb 2014
Letters to Editor
cardiac examination revealed no obvious murmurs, gallops or pericardial rub. The electrocardiogram (ECG) demonstrated normal sinus rhythm with ST segment T wave changes in all leads, which was attributed to tachycardia, hypotension and anaemia. Laboratory results were as follows: Haemoglobin ‑ 5.5 g/dl, haematocrit ‑ 17.6%, total leukocyte count ‑ 14,500/ul, platelet count ‑.2.44 lac/ul, Random Blood Sugar (RBS) ‑ 79 mg/dl, blood urea nitrogen ‑ 23 mg/dl, S.creatinine ‑ 0.79 mg/dl, S.bilirubin ‑ 0.93 mg/dl, serum glutamic oxaloacetic transaminase/serum glutamic pyruvic transaminase ‑ 36/39 IU/L and S.alkaline phosphatase ‑ 369 IU/L. Ultrasonography revealed single intrauterine live foetus of gestational age 34.5 weeks with placenta previa grade 3. Patient received two units of packed red blood cells. Her BP picked up to 106/54 mm Hg on dopamine infusion (7 mcg/kg/min) and was posted for emergency caesarean section. General anaesthesia was planned due to haemodynamic instability of the patient. Rapid sequence induction was performed using propofol 1 mg/kg and ketamine 1 mg/kg and concomitant preoxygenation. Endotracheal intubation was done following injection of succinylcholine 1.5 mg/kg. Patient was maintained on isoflurane 0.7% with O2/N2O (40/60) and atracurium 0.5 mg/kg. Just after delivery of baby, patient developed pulseless ventricular tachycardia. Cardiopulmonary resuscitation was started immediately. Meanwhile, defibrillator was prepared and a shock of 150 joule (biphasic waveform) was delivered. Patient reverted to sinus rhythm, but ST segment elevation appeared on continuous ECG monitoring. Injection oxytocin 10 units was added to 1 L of ringer lactate and given at a rate of 10 ml/min. Patient remained stable during the rest of surgery and was shifted to intensive care unit for elective ventilation and further management. A 12 lead ECG in the immediate post‑operative period showed normal sinus rhythm with ST segment elevation and T wave inversion in lead I, aVL and V1 to V4. Laboratory results were as follows: Troponin I positive; creatinine kinase‑MB fraction ‑ 39 U/L; triglycerides ‑ 310 mg/dL; total cholesterol ‑ 250 mg/dL;high‑density‑lipoprotein‑38 mg/dL and low‑density‑lipoprotein ‑ 163 mg/dL. Cardiologist consultation and bedside echocardiography demonstrated left ventricular wall motion abnormalities at the apex and anterior wall; and ejection fraction of 35 to 40% and mild mitral regurgitation. Patient was treated with aspirin, clopidogrel, unfractionated heparin, Indian Journal of Anaesthesia | Vol. 58| Issue 1 | Jan-Feb 2014
metoprolol and morphine. In the next 24 h patient was weaned off from the ventilator and vasopressor support and was shifted to cardiac catheterization laboratory, where angiography revealed 80% block of left anterior descending artery, but no active intervention was done at that time. Patient was transferred to the cardiac intensive care unit (CICU) and started on a regimen of carvedilol, 12.5 mg; aspirin, 150 mg; clopidogrel, 75 mg; atorvastatin, 20 mg and ivabradine, 7.5 mg. Patient remained stable in CICU and on day 3 she was transferred back to the ward and was discharged on the 7th day with the advice of cardiology follow‑up. The most common underlying mechanisms implicated in AMI during pregnancy are atherosclerotic coronary artery disease (CAD), coronary thrombosis with hypercoagulability and coronary artery dissection. Complications of pregnancy that are significantly associated with AMI are severe anaemia, preeclampsia, postpartum haemorrhage, postpartum infection, shock, ergometrine, prostaglandin E1, fluid and electrolyte imbalances.[2‑5] All causes of tachycardia, hypertension, hypotension, anaemia and pain should be treated aggressively. The interventions include vasopressors to maintain BP, β‑blockers to slow heart rate, managing blood volume, post‑operative pain and respiratory function. Emergent coronary intervention, anticoagulants or glycoprotein IIb/IIIa antagonists are rarely indicated in the immediate post‑operative course and are hazardous because of the risk of bleeding, unless ST elevation or intractable cardiogenic shock ensues.[6] With this case report, we highlight the possibility of presence of unknown CAD and occurrence of perioperative AMI, apart from tachycardia and anaemia in pregnant patients having ST‑T changes in ECG. Tachycardia, hypotension, hypertension, anaemia, hypoxemia and systolic and diastolic myocardial dysfunction are common causes of prolonged ST‑depression and myocardial infarction in patients with stable CAD undergoing major noncardiac surgery. Careful perioperative monitoring for ischemia, a low threshold for treating and preventing tachycardia while avoiding hypotension, decreased cardiac output and/or cardiac decompensation help prevent perioperative myocardial infarction (PMI). Coronary intervention is rarely indicated as the first line of treatment and antithrombotic therapy may exacerbate bleeding. Future studies are needed to determine, which patients with PMI require intensified post‑operative surveillance, 95
Letters to Editor
medical therapy and/or coronary intervention to improve the long‑term survival.
Sadik Mohammed, Rakesh Karnawat, PK Bhatia1, Ghansham Biyani2 Departments of Anaesthesiology, Dr. S. N. Medical College, 1AIIMS, Jodhpur, Rajasthan, 2Department of Anaesthesiology, AIIMS, New Delhi, India Address for correspondence: Dr. Sadik Mohammed, Near Mohammedi Masjid, Hanuman Ji Ki Bhakhari, Nai Sarak, Jodhpur ‑ 342 001, Rajasthan, India. E‑mail: [email protected]
ReferenceS 1.
Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. Ann Intern Med 1996;125:751‑62. 2. James AH, Jamison MG, Biswas MS, Brancazio LR, Swamy GK, Myers ER. Acute myocardial infarction in pregnancy: A United States population‑based study. Circulation 2006;113:1564‑71. 3. Poh CL, Lee CH. Acute myocardial infarction in pregnant women. Ann Acad Med Singapore 2010;39:247‑53. 4. Sutaria N, O'Toole L, Northridge D. Postpartum acute MI following routine ergometrine administration treated successfully by primary PTCA. Heart 2000;83:97‑8. 5. Schulte‑Sasse U. Life threatening myocardial ischaemia associated with the use of prostaglandin E1 to induce abortion. BJOG 2000;107:700‑2. 6. Berger PB, Bellot V, Bell MR, Horlocker TT, Rihal CS, Hallett JW, et al. An immediate invasive strategy for the treatment of acute myocardial infarction early after noncardiac surgery. Am J Cardiol 2001;87:1100‑2, A6, A9. Access this article online Quick response code Website: www.ijaweb.org
DOI: 10.4103/0019-5049.126846
Dexmedetomidine in the management of severe tetanus Sir, Although tetanus is a rare disease in the developed countries now, it remains a significant cause of death world-wide and is associated with a high rate of mortality. Components of severe tetanus management are supportive care with sedation, airway protection and controlled ventilation.[1] Dexmedetomidine is a high selective α-2-receptor agonist. It has combined analgesic and anti-sympathetic effect without respiratory system depression. There have been several studies describing its successful use in 96
mechanically ventilated patients for short- (24 h) and long-term (up to 7 days) use in the intensive care unit (ICU).[2] Dexmedetomidine has been also used in the treatment of tetanus in six patients for 7 days.[3] We present a case of generalised tetanus complicated by uncontrolled sympathetic over activity (SOA) managed with dexmedetomidine infusion. A 53-year-old male patient presented with complaints of dyspnoea, upper lip twitching, difficulty in swallowing and a local abscess around his right foot. He had a medical history of penetrating wound in his right foot 11 days before. Antibiotics and human tetanus immunoglobulin were administered and the wound was surgically debrided. Because of respiratory failure with SOA, he was intubated and mechanically ventilated. SOA persisted despite midazolam and magnesium sulphate infusion. Dexmedetomidine infusion was started on day 5 and SOA could be controlled successfully. On day 10, severe bronchopneumonia developed and the patient died on day 12. The management of tetanus requires the prevention of tetanospasmin absorption, treatment of symptoms, stabilisation of autonomic instability, antibiotic therapy and control of the airway with assisted ventilation if indicated. Basal SOA is characterised by resting tachycardia and depression of bowel motility and bladder function, while severe SOA presents with fluctuating tachycardia, labile hypertension and sweating with and without stimulation.[4] Different methods to control SOA have been provided, including magnesium sulphate infusions, dantrolene infusions, intrathecal administration of baclofen, benzodiazepine, clonidine and dexmedetomidine.[5] Girgin et al.[3] reported use of dexmedetomidine in the management of tetanus for 7 days in six patients without any side-effects. According to the same author, its administration did not fully control the muscle spasm, but decreased their frequency and severity and reduced the use of sedative drugs to control muscle spasms and cardiovascular instability. In this case, we started dexmedetomidine infusion on the 5th day in the ICU, because midazolam and magnesium sulphate infusions did not efficiently control SOA. We observed that tachycardia (heart rate >110 beats/ min) and hypertension (mean arterial blood pressure >100 mmHg) decreased to acceptable normal levels and need for sedative drugs was reduced after starting dexmedetomidine infusion. However, we were not able to fully avoid their use. We used dexmedetomidine for 4 days. Although hypotension and bradycardia are the Indian Journal of Anaesthesia | Vol. 58| Issue 1 | Jan-Feb 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.
