CASE REPORT
I11
Peri-Partum Pulmonary Oedema SHANITAN* Department of Anaesthesia and Intensive Care, Singapore General Hospital Key Words: ANAESTHESIA: obstetric; pre-term labour, beta-2 agonist therapy, acute pulmonary oedema
CASE REPORT A 34-year-old Chinese female, G3, P2, was transferred to the labour ward from another hospital with the following problems: a history of two previous caesarean sections for cephalopelvic disproportion, pre-term labour at 27 weeks, low lying placenta and anaemia (haemoglobin 7.4 gldl), She weighed 60 kg and was 1.47 m in height, A transfusion of whole blood was started prior to transfer; 420 ml had been given by the time she was admitted to the labour ward and another 500 ml was given over the next two hours, As she was having uterine contractions once every two minutes, a salbutamol infusion which had been started prior to transfer at a rate of 1.6 mcglmin was increased to I 7 mcglmin, Her blood pressure (BP) and heart rate (HR) at that time were 106/63 mmHg and 102/min respectively. An obstetric review six hours later showed that uterine contractions had ceased and a foetal tachycardia (I 75/min baseline) was noted. Another two packs of whole blood totalling 970 ml (420 + 550) were ordered to be transfused over the next fourteen hours. Ten hours after transfer, the patient complained of palpitations. Her HR then was 1311 min and her BP 105/51 mmHg. The salbutamol infusion was reduced to 8 mcglmin and gradually reduced and was stopped twenty hours after admission. Oral salbutamol therapy at 4 mg tds was commenced. Unfortunately, 27 hours after admission, the patient had spontaneous rupture of membranes and a decision was made to proceed with an emergency lower segment caesarean section (LSCS) which was carried out an hour later. She was afebrile. Oral sodium citrate 20 ml 0.3M was given prior to transfer to the operating theatre. Routine monitoring of electrocardiograph (ECG), noninvasive blood pressure (NIBP, Dinamap, Critikon) and pulse oximetry (Ohmeda Biox 3701) ·M.B.B.S., F.FAR.C.S., Senior Registrar. Address fOT reprints: Shani Tan, Senior Registrar, Department of Anaesthesia and Intensive Care, Singapore General Hospital, Outram Road, Singapore 0316. Republic of Singapore. Accepted for publication October 2, 1990 Anaesthesia and Intensive Care. Vol. 19, No. 1, February. 1991
was commenced. Immediate preinduction BP was 110/60 mmHg and HR was 115/min. The pulse oximeter reading was 99% saturation (Sa02). She was preoxygenated with F Io 2 1.0 and a rapidsequence induction with cricoid pressure was carried out using sodium thiopentone 300 mg and suxamethonium lOO mg. No atropine was given. She was intubated without difficulty using a 6.5 mm cuffed oral endotracheal tube. The anaesthetist at the time noted that the oropharynx was dry. Intermittent positive pressure ventilation with 50% nitrous oxide in oxygen and 0.5% halothane was commenced and high airway pressures of 40 to 50 cm H 20 were observed. Auscultation of the lungs revealed equal air entry but there was severe bronchospasm with widespread rhonchi and crepitations bilaterally. Two possible causes were considered by the anaesthetist at that time - aspiration of gastric contents or acute asthmatic attack. A bolus dose of aminophylline 125 mg IV was followed by an infusion of aminophylline 250 mg in normal saline 500 ml over six hours. Intravenous hydrocortisone hemisuccinate 200 mg was also given with some improvement of the bronchospasm. Due to previous surgery, there were extensive adhesions and the operation lasted approximately two hours. Intravenous oxytocin 10 IU was given after delivery. A total of 1.5 litres of Hartmann's solution was infused intraoperatively: blood loss was recorded as 500 ml, urine output 300 ml. The patient remained cardiovascularly stable but unfortunately no further record of haemoglobin saturation was made in the anaesthetic record chart. At the end of the operation the patient was not reversed and extubated but sent to the Surgical Intensive Care Unit (SICU) for further management. A clinical diagnosis of acute pulmonary oedema was made. This was confirmed by chest X-ray. A twelve-lead electrocardiogram was normal. There were two possible contributory causes for her condition - a positive fluid balance of 3.72 litres since admission 36 hours before and beta-2 agonist therapy for pre-term labour. The patient was
112
SHANITAN
support and most responded promptly to withdrawal of the beta-2 sympathomimetic agent and the administration of oxygen therapy and diuretics. The patient reported here developed signs of acute pulmonary oedema immediately after intubation and the pulmonary changes were severe enough to warrant postoperative ventilation for 24 hours. The patient probably had some symptoms of incipient heart failure preoperatively: on direct questioning she admitted to having palpitations and 'tightness in the chest' a few hours before the caesarean section. Several contributory factors are present in this case. There was a large positive fluid balance of 3.72 litres preoperatively (which consisted of 1910 ml of whole blood, 2000 ml of Hartmann's solution, 800 ml of normal saline, 1010 ml of dextrose 5% (in which salbutamol was delivered), and an oral intake of 500 ml balanced against a urine output of 2500 ml). Cardiovascular effects of beta-2 agonist therapy and possibly additional tachycardia occurring at the time of induction may have precipitated the onset of frank pulmonary oedema. This is in contrast to a patient reported by KnightS in whom cardiac status deteriorated in the third stage following administration of oxytoxin. Supporting the hypothesis of fluid overload and beta-2 agonist as a cause is the rapid recovery after the withdrawal of salbutamol and a brisk diuresis with the administration of diuretics. A 2-D echocardiogram carried out on the sixth postoperative day excluded any pre-existing heart disease. Various mechanisms have been proposed for the development of pulmonary oedema associated with beta-2 sympathomimetic therapy. These include fluid overload (especially with 5% dextrose DISCUSSION solution),6,9 catecholamine-related myocardial Acute pulmonary oedema is an uncommon but potentially fatal complication of beta-2 agonist necrosislo,116 and cardiac failure secondary to ,12 which would lead to pulmonary therapy for pre-term labour. The first case was tachycardia 13 oedema published in 1977. 1 Since then, over seventy cases oedema. Non-cardiogenic pulmonary 14 Myocardial has been reported in a review. have been reported. The agents implicated have been terbutaline, 2 ritodrine,3 isoxuprine, 4 ischaemia as evidenced by electrocardiographic 2 salbutamol 5 and fenoterol. 6 Approximately 10% of changes has also been reported. Apart from pulmonary oedema, the other these patients died as a result of beta-2 agonist therapy. There has been no correlation between the complications of maternal beta-2 agonist therapy total dose, duration, or route of administration may be divided into maternal and foetal. The with the likelihood of developing pulmonary maternal side-effects include cardiovascular oedema. 7 In a review 7 of cases of pulmonary changes (beta-2 agonists accentuate some normal oedema associated with beta agonist therapy, in physiological changes of pregnancy, i.e. an increase 63% of cases reported pulmonary oedema occurred in heart rate, cardiac output and a decrease in before delivery. Of those that developed systemic vascular resistance), hypokalaemia, pulmonary oedema post delivery, 11.7% (2117) hyperglycaemia, anxiety, arousal and muscle occurred after general anaesthesia for caesarean tremor. Foetal tachycardia and hypoglycaemia 15 section. A similar number were reported to have have been reported. Various recommendations have been made developed pulmonary oedema following epidural anaesthesia. Only a minority required ventilatory regarding the perioperative management of
sedated and mechanically ventilated and intravenous frusemide 80 mg was given. A central venous catheter inserted approximately two hours postoperatively showed a central venous pressure (CVP) of 17 cm H20. An arterial blood gas sample taken two hours later showed pH 7.478, PC02 31.3 mmHg (4.17 kPa), P02 101.7 mmHg (13.56 kPa), base excess (BE) 0.1, Sao2 97.6%, standard bicarbonate (SBC) 24.5 with a ventilator setting ofSIMV 12/min, FI02 0.6 and PEEP + 5 cm H 20. Postoperative haemoglobin was 9.0 gldl, urea 1.6 mmolll, sodium (Na + ) 138 mmol/l, potassium (K + ) 4.1 mmolll, glucose 7.1 mmol/l, creatinine 39 mmolll. No blood transfusion was given postoperatively. By twelve hours postoperatively, the patient, now awake and alert, showed much improvement. She felt subjectively better and there was marked reduction in the auscultatory signs in the lungs with no more rhonchi and mimimal crepitations. Her cardiovascular status remained stable with a BP of 105170 mmHg, HR 94/min and CVP had fallen to + 3 to + 4 mmHg. She produced 3.0 litres of urine over the twelve hours. She was gradually weaned off the ventilator. An arterial blood gas analysis twelve hours postoperatively showed pH 7.504, PC02 28 mmHg (3.73 kPa), P02 158.4 mmHg (21.12 kPa), BE -0.4, Sao2 99.3, SBC 24.0 with a ventilator setting of F Io 2 0.35, SIMV 6/min and PEEP + 5 cm H 20. She was extubated thirty hours postoperatively. She remained well and was transferred to the postnatal ward where the rest of her stay was uneventful. A 2-D echocardiogram done on the sixth postoperative day was normal and she was discharged from hospital the following day.
Anaesthesia and Intensive Care, Vol. 19. No. 1. FebrtlfJry. 1991
113
CASE REPORT
patients receiving beta-2 agonist therapy for preterm labour. Preoperatively there should be a high index of suspicion with respect to pulmonary oedema. Fluid balance and electrolytes must be carefully monitored as a large amount of 5% dextrose solution may be given as a carrier for the beta-2 agonist. Blood sugar levels should also be monitored. As oxygen consumption is increased, these patients should receive supplemental oxygen while in the labour ward. If there is suspicion of pulmonary oedema or symptoms of myocardial ischaemia or arrythymia, a twelve-lead ECG should be done. Intraoperative management is tailored to the patient's clinical condition. In the absence of frank pulmonary oedema, routine monitoring of ECG, NIBP, capnography and pulse oximetry suffices. In the presence of frank pulmonary oedema, invasive arterial and central venous pressure monitoring should be used. Thiopentone would appear to be a suitable induction agent while ketamine or cyclopropane are contraindicated because they would increase sympathetic tone further. Some have advocated the use of enflurane or isoflurane instead of halothane to supplement anaesthesia and prevent awareness as the former produce less myocardial depression. 15.16 Oxytocin is given in preference to ergometrine. As these patients often present as an emergency, there is usually little time for a regional anaesthetic technique. However, in the event that a regional is required, an epidural with careful titration of sensory level is advised. There should be close monitoring of cardiovascular parameters with judicious fluid loading taking into consideration preoperative fluid balance. In conclusion, pulmonary oedema is an uncommon complication of therapy for a common problem; twenty to thirty per cent of all pregnancies more than twenty weeks suffer 'threatened' premature labour. An awareness of the side-effects of maternal beta-2 agonist therapy will aid perioperative management of such patients.
ACKNOWLEDGEMENTS
I would like to thank Dr. T. H. Ho for permission to report this patient.
Anaesthesia and Intensive Care, Vol. 19, No. I, February, 1991
REFERENCES
1, Kubli F. Proceedings of the study group on pre-term labour. A Anderson, ed. Roy Coli Obst Gyn 1977; 218-220. 2. Katz M, Robertson PA, Creasy RK. Cardiovascular complications associated with terbutaline treatment for preterm labour. Am J Obst Gynecol 1981; 139:605-608. 3. Abramorici H, Lewin A, Lissak A, Palant A. Maternal pulmonary oedema occurring after therapy with ritodrine for premature uterine contractions. Acta Ob stet Gynecol Scand 1980; 59:555. 4. Nagey DA, Crenshaw MC. Pulmonary complications of isoxuprine therapy in the gravida. Obstet Gynecol 1981; 59 Supp: 33S-42S. 5. Davies A, Robertson MJS. Pulmonary oedema after the administration of intravenous salbutamol and ergometrine. Case Report. Br J Obstet Gynecol 1980; 87:539-541. 6. Guernsey BG, Villareal Y, Snyder MD, Gabert HA. Pulmonary oedema associated with the use of betamimetic agents in preterm labour. Am J Hosp Pharm 1981; 88: 1942-8. 7. Hawker F. Pulmonary oedema associated with beta-2 sympthomimetic treatment of premature labour. Anaesth Intens care 1984; 12: 143-151. 8. Crowhurst JA. Salbutamol, Obstetrics and Anaesthesia: A Review and Case Discussion. Anaesth Intens Care 1980; 8:39-43. 9. Ellcolt HR, Abdulla U. Pulmonary oedema associated with ritodrine infusion and betamethasone administration in premature labour. Br Med J 1978; 2:799-780. 10. Miliez J, Gureau C. A case report of maternal death associated with betamimetics and betamethasone in premature labour. Europ J Obstet Gynae Reprod Bioi 1980; 11:95-100. I!. Van Vliety PO, Burchell HB, Titus JL. Focal myocarditis associated with phaeochromocytoma. N Engl J Med 1966; 274:1102-1108. 12. Ravindran R, Viegas OJ, Padilla LM, La Blond P. Anaesthetic considerations in pregnant patients receiving terbutaline therapy. Anaesth Analg 1980; 59:391-392. 13. Wheeler AS, Patel KF, Spain J. Pulmonary oedema during beta-2 tocolytic therapy. Anaesth Analg 1981; 60:695-696. 14. Benedetti TJ, Hargrove JC, Rosene KA. Maternal pulmonary edema during premature labor inhibition. Obstet Gynecol1982; 59 Suppl: 33S-37S. 15. Cook P. Beta-2 agonists in obstetrics: The anaesthetic implications, Kerr OR, ed. Australian Anaesthesia 1988, Faculty of Anaesthetists, Royal Australasian College of Surgeons: 14-20. 16. Stoeling RK. Sympathetic nervous system: function and clinical phamacology. In: ASA Refresher Courses in Anaesthesiology. JB Lippincott Co., U.S.A. 1977; 5:15:201.
I11
Peri-Partum Pulmonary Oedema SHANITAN* Department of Anaesthesia and Intensive Care, Singapore General Hospital Key Words: ANAESTHESIA: obstetric; pre-term labour, beta-2 agonist therapy, acute pulmonary oedema
CASE REPORT A 34-year-old Chinese female, G3, P2, was transferred to the labour ward from another hospital with the following problems: a history of two previous caesarean sections for cephalopelvic disproportion, pre-term labour at 27 weeks, low lying placenta and anaemia (haemoglobin 7.4 gldl), She weighed 60 kg and was 1.47 m in height, A transfusion of whole blood was started prior to transfer; 420 ml had been given by the time she was admitted to the labour ward and another 500 ml was given over the next two hours, As she was having uterine contractions once every two minutes, a salbutamol infusion which had been started prior to transfer at a rate of 1.6 mcglmin was increased to I 7 mcglmin, Her blood pressure (BP) and heart rate (HR) at that time were 106/63 mmHg and 102/min respectively. An obstetric review six hours later showed that uterine contractions had ceased and a foetal tachycardia (I 75/min baseline) was noted. Another two packs of whole blood totalling 970 ml (420 + 550) were ordered to be transfused over the next fourteen hours. Ten hours after transfer, the patient complained of palpitations. Her HR then was 1311 min and her BP 105/51 mmHg. The salbutamol infusion was reduced to 8 mcglmin and gradually reduced and was stopped twenty hours after admission. Oral salbutamol therapy at 4 mg tds was commenced. Unfortunately, 27 hours after admission, the patient had spontaneous rupture of membranes and a decision was made to proceed with an emergency lower segment caesarean section (LSCS) which was carried out an hour later. She was afebrile. Oral sodium citrate 20 ml 0.3M was given prior to transfer to the operating theatre. Routine monitoring of electrocardiograph (ECG), noninvasive blood pressure (NIBP, Dinamap, Critikon) and pulse oximetry (Ohmeda Biox 3701) ·M.B.B.S., F.FAR.C.S., Senior Registrar. Address fOT reprints: Shani Tan, Senior Registrar, Department of Anaesthesia and Intensive Care, Singapore General Hospital, Outram Road, Singapore 0316. Republic of Singapore. Accepted for publication October 2, 1990 Anaesthesia and Intensive Care. Vol. 19, No. 1, February. 1991
was commenced. Immediate preinduction BP was 110/60 mmHg and HR was 115/min. The pulse oximeter reading was 99% saturation (Sa02). She was preoxygenated with F Io 2 1.0 and a rapidsequence induction with cricoid pressure was carried out using sodium thiopentone 300 mg and suxamethonium lOO mg. No atropine was given. She was intubated without difficulty using a 6.5 mm cuffed oral endotracheal tube. The anaesthetist at the time noted that the oropharynx was dry. Intermittent positive pressure ventilation with 50% nitrous oxide in oxygen and 0.5% halothane was commenced and high airway pressures of 40 to 50 cm H 20 were observed. Auscultation of the lungs revealed equal air entry but there was severe bronchospasm with widespread rhonchi and crepitations bilaterally. Two possible causes were considered by the anaesthetist at that time - aspiration of gastric contents or acute asthmatic attack. A bolus dose of aminophylline 125 mg IV was followed by an infusion of aminophylline 250 mg in normal saline 500 ml over six hours. Intravenous hydrocortisone hemisuccinate 200 mg was also given with some improvement of the bronchospasm. Due to previous surgery, there were extensive adhesions and the operation lasted approximately two hours. Intravenous oxytocin 10 IU was given after delivery. A total of 1.5 litres of Hartmann's solution was infused intraoperatively: blood loss was recorded as 500 ml, urine output 300 ml. The patient remained cardiovascularly stable but unfortunately no further record of haemoglobin saturation was made in the anaesthetic record chart. At the end of the operation the patient was not reversed and extubated but sent to the Surgical Intensive Care Unit (SICU) for further management. A clinical diagnosis of acute pulmonary oedema was made. This was confirmed by chest X-ray. A twelve-lead electrocardiogram was normal. There were two possible contributory causes for her condition - a positive fluid balance of 3.72 litres since admission 36 hours before and beta-2 agonist therapy for pre-term labour. The patient was
112
SHANITAN
support and most responded promptly to withdrawal of the beta-2 sympathomimetic agent and the administration of oxygen therapy and diuretics. The patient reported here developed signs of acute pulmonary oedema immediately after intubation and the pulmonary changes were severe enough to warrant postoperative ventilation for 24 hours. The patient probably had some symptoms of incipient heart failure preoperatively: on direct questioning she admitted to having palpitations and 'tightness in the chest' a few hours before the caesarean section. Several contributory factors are present in this case. There was a large positive fluid balance of 3.72 litres preoperatively (which consisted of 1910 ml of whole blood, 2000 ml of Hartmann's solution, 800 ml of normal saline, 1010 ml of dextrose 5% (in which salbutamol was delivered), and an oral intake of 500 ml balanced against a urine output of 2500 ml). Cardiovascular effects of beta-2 agonist therapy and possibly additional tachycardia occurring at the time of induction may have precipitated the onset of frank pulmonary oedema. This is in contrast to a patient reported by KnightS in whom cardiac status deteriorated in the third stage following administration of oxytoxin. Supporting the hypothesis of fluid overload and beta-2 agonist as a cause is the rapid recovery after the withdrawal of salbutamol and a brisk diuresis with the administration of diuretics. A 2-D echocardiogram carried out on the sixth postoperative day excluded any pre-existing heart disease. Various mechanisms have been proposed for the development of pulmonary oedema associated with beta-2 sympathomimetic therapy. These include fluid overload (especially with 5% dextrose DISCUSSION solution),6,9 catecholamine-related myocardial Acute pulmonary oedema is an uncommon but potentially fatal complication of beta-2 agonist necrosislo,116 and cardiac failure secondary to ,12 which would lead to pulmonary therapy for pre-term labour. The first case was tachycardia 13 oedema published in 1977. 1 Since then, over seventy cases oedema. Non-cardiogenic pulmonary 14 Myocardial has been reported in a review. have been reported. The agents implicated have been terbutaline, 2 ritodrine,3 isoxuprine, 4 ischaemia as evidenced by electrocardiographic 2 salbutamol 5 and fenoterol. 6 Approximately 10% of changes has also been reported. Apart from pulmonary oedema, the other these patients died as a result of beta-2 agonist therapy. There has been no correlation between the complications of maternal beta-2 agonist therapy total dose, duration, or route of administration may be divided into maternal and foetal. The with the likelihood of developing pulmonary maternal side-effects include cardiovascular oedema. 7 In a review 7 of cases of pulmonary changes (beta-2 agonists accentuate some normal oedema associated with beta agonist therapy, in physiological changes of pregnancy, i.e. an increase 63% of cases reported pulmonary oedema occurred in heart rate, cardiac output and a decrease in before delivery. Of those that developed systemic vascular resistance), hypokalaemia, pulmonary oedema post delivery, 11.7% (2117) hyperglycaemia, anxiety, arousal and muscle occurred after general anaesthesia for caesarean tremor. Foetal tachycardia and hypoglycaemia 15 section. A similar number were reported to have have been reported. Various recommendations have been made developed pulmonary oedema following epidural anaesthesia. Only a minority required ventilatory regarding the perioperative management of
sedated and mechanically ventilated and intravenous frusemide 80 mg was given. A central venous catheter inserted approximately two hours postoperatively showed a central venous pressure (CVP) of 17 cm H20. An arterial blood gas sample taken two hours later showed pH 7.478, PC02 31.3 mmHg (4.17 kPa), P02 101.7 mmHg (13.56 kPa), base excess (BE) 0.1, Sao2 97.6%, standard bicarbonate (SBC) 24.5 with a ventilator setting ofSIMV 12/min, FI02 0.6 and PEEP + 5 cm H 20. Postoperative haemoglobin was 9.0 gldl, urea 1.6 mmolll, sodium (Na + ) 138 mmol/l, potassium (K + ) 4.1 mmolll, glucose 7.1 mmol/l, creatinine 39 mmolll. No blood transfusion was given postoperatively. By twelve hours postoperatively, the patient, now awake and alert, showed much improvement. She felt subjectively better and there was marked reduction in the auscultatory signs in the lungs with no more rhonchi and mimimal crepitations. Her cardiovascular status remained stable with a BP of 105170 mmHg, HR 94/min and CVP had fallen to + 3 to + 4 mmHg. She produced 3.0 litres of urine over the twelve hours. She was gradually weaned off the ventilator. An arterial blood gas analysis twelve hours postoperatively showed pH 7.504, PC02 28 mmHg (3.73 kPa), P02 158.4 mmHg (21.12 kPa), BE -0.4, Sao2 99.3, SBC 24.0 with a ventilator setting of F Io 2 0.35, SIMV 6/min and PEEP + 5 cm H 20. She was extubated thirty hours postoperatively. She remained well and was transferred to the postnatal ward where the rest of her stay was uneventful. A 2-D echocardiogram done on the sixth postoperative day was normal and she was discharged from hospital the following day.
Anaesthesia and Intensive Care, Vol. 19. No. 1. FebrtlfJry. 1991
113
CASE REPORT
patients receiving beta-2 agonist therapy for preterm labour. Preoperatively there should be a high index of suspicion with respect to pulmonary oedema. Fluid balance and electrolytes must be carefully monitored as a large amount of 5% dextrose solution may be given as a carrier for the beta-2 agonist. Blood sugar levels should also be monitored. As oxygen consumption is increased, these patients should receive supplemental oxygen while in the labour ward. If there is suspicion of pulmonary oedema or symptoms of myocardial ischaemia or arrythymia, a twelve-lead ECG should be done. Intraoperative management is tailored to the patient's clinical condition. In the absence of frank pulmonary oedema, routine monitoring of ECG, NIBP, capnography and pulse oximetry suffices. In the presence of frank pulmonary oedema, invasive arterial and central venous pressure monitoring should be used. Thiopentone would appear to be a suitable induction agent while ketamine or cyclopropane are contraindicated because they would increase sympathetic tone further. Some have advocated the use of enflurane or isoflurane instead of halothane to supplement anaesthesia and prevent awareness as the former produce less myocardial depression. 15.16 Oxytocin is given in preference to ergometrine. As these patients often present as an emergency, there is usually little time for a regional anaesthetic technique. However, in the event that a regional is required, an epidural with careful titration of sensory level is advised. There should be close monitoring of cardiovascular parameters with judicious fluid loading taking into consideration preoperative fluid balance. In conclusion, pulmonary oedema is an uncommon complication of therapy for a common problem; twenty to thirty per cent of all pregnancies more than twenty weeks suffer 'threatened' premature labour. An awareness of the side-effects of maternal beta-2 agonist therapy will aid perioperative management of such patients.
ACKNOWLEDGEMENTS
I would like to thank Dr. T. H. Ho for permission to report this patient.
Anaesthesia and Intensive Care, Vol. 19, No. I, February, 1991
REFERENCES
1, Kubli F. Proceedings of the study group on pre-term labour. A Anderson, ed. Roy Coli Obst Gyn 1977; 218-220. 2. Katz M, Robertson PA, Creasy RK. Cardiovascular complications associated with terbutaline treatment for preterm labour. Am J Obst Gynecol 1981; 139:605-608. 3. Abramorici H, Lewin A, Lissak A, Palant A. Maternal pulmonary oedema occurring after therapy with ritodrine for premature uterine contractions. Acta Ob stet Gynecol Scand 1980; 59:555. 4. Nagey DA, Crenshaw MC. Pulmonary complications of isoxuprine therapy in the gravida. Obstet Gynecol 1981; 59 Supp: 33S-42S. 5. Davies A, Robertson MJS. Pulmonary oedema after the administration of intravenous salbutamol and ergometrine. Case Report. Br J Obstet Gynecol 1980; 87:539-541. 6. Guernsey BG, Villareal Y, Snyder MD, Gabert HA. Pulmonary oedema associated with the use of betamimetic agents in preterm labour. Am J Hosp Pharm 1981; 88: 1942-8. 7. Hawker F. Pulmonary oedema associated with beta-2 sympthomimetic treatment of premature labour. Anaesth Intens care 1984; 12: 143-151. 8. Crowhurst JA. Salbutamol, Obstetrics and Anaesthesia: A Review and Case Discussion. Anaesth Intens Care 1980; 8:39-43. 9. Ellcolt HR, Abdulla U. Pulmonary oedema associated with ritodrine infusion and betamethasone administration in premature labour. Br Med J 1978; 2:799-780. 10. Miliez J, Gureau C. A case report of maternal death associated with betamimetics and betamethasone in premature labour. Europ J Obstet Gynae Reprod Bioi 1980; 11:95-100. I!. Van Vliety PO, Burchell HB, Titus JL. Focal myocarditis associated with phaeochromocytoma. N Engl J Med 1966; 274:1102-1108. 12. Ravindran R, Viegas OJ, Padilla LM, La Blond P. Anaesthetic considerations in pregnant patients receiving terbutaline therapy. Anaesth Analg 1980; 59:391-392. 13. Wheeler AS, Patel KF, Spain J. Pulmonary oedema during beta-2 tocolytic therapy. Anaesth Analg 1981; 60:695-696. 14. Benedetti TJ, Hargrove JC, Rosene KA. Maternal pulmonary edema during premature labor inhibition. Obstet Gynecol1982; 59 Suppl: 33S-37S. 15. Cook P. Beta-2 agonists in obstetrics: The anaesthetic implications, Kerr OR, ed. Australian Anaesthesia 1988, Faculty of Anaesthetists, Royal Australasian College of Surgeons: 14-20. 16. Stoeling RK. Sympathetic nervous system: function and clinical phamacology. In: ASA Refresher Courses in Anaesthesiology. JB Lippincott Co., U.S.A. 1977; 5:15:201.
