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Correspondence The patient may complain of a heavy lid or difficulty in breathing through the nose because of a congested mucosa. It may go completely unnoticed by the patient and be observed by the midwife or the anaesthetist. Bilateral Horner’s syndrome is even less noticeable. All that the patient needs is reassurance as recovery is complete once the local anaesthetic wears off. Burn et al.6 used epidurograms to show that volumes greater than 40 mL injected in the lumbar or caudal region can reach the thoracic and lower cervical segments. Bromage7 postulated that the use of oxytocin in labour predisposed to Horner’s syndrome. The volume and type or concentration of local anaesthetic, or the height reached, are not predictive for the occurrence of the syndrome. Neither the use of oxytocin nor the fact that the patient is in labour bears any relation to the syndrome. G. R. Simon Heartlands and Solihull Hospitals NHS Trust, Birmingham, UK K. C. Clayton Walsgrave Hospitals NHS Trust, Coventry, UK REFERENCES 1. Kepes E R, Martinez L R, Pantuck E, et al. Horner’s syndrome following caudal anaesthesia. NY J Med 1972; 72: 946–947. 2. Skaerdoff M N, Datta S. Horner’s syndrome during epidural anaesthesia for elective Caesarean section. Can Anaesth Soc J 1981; 28: 82–85. 3. Clayton K C. The incidence of Horner’s syndrome during lumbar extradural for elective Caesarean section and provision of analgesia during labour. Anaesthesia 1983; 38: 583–585. 4. Paw H G. Horner’s syndrome following low-dose epidural infusion for labour: a cautionary tale. Eur J Anaesth 1998; 15: 110–111. 5. Hertz R, Chiovari C A, Marx G F. Delayed Horner’s syndrome following obstetric extradural block. Anesth Analg 1980; 59: 299–300. 6. Burn J M, Guyer P B, Langdon L. The spread of solutions injected into the epidural space. Br J Anaesth 1973; 45: 338–345. 7. Bromage P R. Epidural Analgesia. Philadelphia: WB Saunders Co, 1978: 588.
doi: 10.1054/ijoa.2001.0838
Transposition of the great vessels: more experience I was interested to read the article by Yarrow and Russell on transposition of the great vessels in the June 2000 issue of IJOA.1 At the time I was involved in the care of a 29-year-old woman with surgically corrected transposition of the great vessels awaiting her fifth delivery. This woman has had more deliveries than any of those documented by Yarrow and Russell, and may therefore be of interest to others. The patient was born in 1970 and at 5 weeks of age her cyanotic spells were diagnosed as transposition of
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the great vessels with patent ductus arteriosus. She initially had balloon septostomy and then closure of patent ductus arteriosus. In 1976 she had a Mustard atrial baffle repair. In 1981 she was admitted with rheumatic fever with carditis (fever, joint pain, raised ASO titre and changed murmur). She had subsequent admissions for ‘collapse’ associated with minor injuries, when she was noted to be bradycardic with a heart rate 38–40 bpm. It was considered that she might need a pacemaker in the future. In 1990 at the age of 19 years, she presented at another hospital for antenatal assessment in her first pregnancy. The case was reviewed by the cardiologist at 32 weeks’ gestation and she was noted to have a grade 2/6 midsystolic murmur over the sternum, and grade 2/6 blowing systolic murmur at the apex, with BP 125/80 mmHg. Her ECG showed sinus arrhythmia, right axis deviation and right ventricular hypertrophy. Chest Xray showed a cardiothoracic ratio of 55% and no evidence of congestive heart failure. She was admitted in spontaneous labour at 38 weeks’ gestation with preeclampsia, a diastolic pressure of 120 mmHg and 3+ proteinuria. Epidural analgesia was established with bupivacaine 0.5%, and two further top-ups were given. She was breathless and tachycardic during the second stage so the baby was delivered by elective outlet forceps. She remained hypertensive for 10 days post partum, and had evidence of congestive heart failure on day 6. She was eventually discharged home on day 13. She presented in her second pregnancy in 1992 with spontaneous onset of labour, and was admitted at 2 cm cervical dilatation. Epidural analgesia was established with bupivacaine 0.5% 10 mL, with one further top-up of bupivacaine 0.375% 8 mL. Outlet forceps delivery was carried out electively 8 h after admission. She had no post-partum complications and was discharged on day 5. In 1994, the patient was admitted to hospital after collapse at home. She had sepsis related to dental caries. Again she was noted to be bradycardic with heart rate of 40 bpm. In 1996 she had a miscarriage at 6 weeks. Preoperative ECG showed bradycardia of 38 bpm, right axis deviation and right ventricular hypertrophy as before. She first presented at our hospital in 1997. She was seen at antenatal clinic at 27 week’ gestation. She was admitted in spontaneous labour at 41 weeks’ gestation and epidural analgesia was established 2 h after admission, with bupivacaine 0.375% 10 mL plus fentanyl 50 µg, followed by infusion of bupivacaine 0.125% with fentanyl 2 µg/mL at 10 mL/h. She had a spontaneous vaginal delivery after 45 min in second stage. In her fifth pregnancy she was seen antenatally at 32 weeks’ gestation. She was admitted in spontaneous
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International Journal of Obstetric Anesthesia
labour at 39 weeks’ gestation and 4 cm cervical dilatation. Epidural analgesia was requested but she reached full cervical dilatation and delivered spontaneously minutes later. She went home after 24 h. In her most recent pregnancy she was referred early to both anaesthetist (EL) and cardiologist. At 32 weeks she was noted to be tired with occasional palpitations but not short of breath. She had mild ankle oedema but no evidence of congestive heart failure. ECG showed sinus rhythm 66 bpm with occasional ectopic beats, and right ventricular hypertrophy. Her echocardiogram showed fractional shortening of right ventricle of 20%. At 38 weeks she was very tired with some breathlessness climbing stairs and hypotension (systolic 90 mmHg). Arrangements were made for close monitoring during labour, and early epidural analgesia. She was admitted in spontaneous labour at 40 weeks, transferred to the intensive care unit, and an epidural was placed 2 h later with ropivacaine 0.2% 10 mL and fentanyl 100 µg, followed by infusion of ropivacaine 0.2% at 6–8 mL/h. ECG, pulse oximetry and invasive blood pressure were monitored. She required Syntocinon infusion to augment labour, but had a rapid second stage of 12 min, and spontaneous vaginal delivery 7 h after admission. She showed no signs of heart failure. All deliveries and surgical interventions were covered with appropriate antibiotic prophylaxis and Syntocinon was given after each delivery. All her children are healthy. The patient has just had laparoscopic tubal ligation 6 weeks post partum, complicated by bradycardia to 28 bpm in the recovery period. E. Langton Department of Anaesthesia, Palmerston North Hospital, Palmerston North, New Zealand REFERENCE 1. Yarrow S, Russell R. Transposition of the great vessels: a series of three cases with a review of the literature. International Journal of Obstetric Anesthesia 2000; 9: 179–185.
doi: 10.1054/ijoa.2001.0839
CSE is the regional anaesthetic technique of choice for placenta praevia We read with interest the case report of a parturient with bleeding placenta praevia and a potentially malignant hyperthermia-susceptible fetus.1 We wonder why a combined spinal epidural (CSE) was not the method of anaesthesia chosen, as prolongation of surgery was a possibility and in a worse case scenario1 an obstetric hysterectomy might have been needed. In a review by Chestnut et al. of obstetric
hysterectomies,2 conversion to general anaesthesia was needed at 75 min in one case due to inadequate block. Also the mean operating time was over 2 h in his series of 46 patients. I appreciate that general anaesthesia could have been administered once the fetus was delivered but this is not an ideal situation. We recently performed a caesarean section on a patient with a grade 4 placenta praevia under CSE. After delivery there was major haemorrhage from the lower segment with a measured blood loss of 6 L in the space of an hour. A modified B-Lynch suture secured haemostasis. This required extensive uterine manipulation and exteriorisation. At no time was the patient hypotensive and she was happy to be awake throughout the procedure. At one stage while waiting for more blood (she had already had the 4 units crossmatched for her) we estimated that her haemoglobin was around 5 g/dL. Despite this she was co-operative and her husband remained with her throughout the procedure, both having been warned preoperatively about the possibility of major haemorrhage. Keeping her awake provided us with a valuable cerebral monitor, which would not have been available to us had she been asleep. In total she received 10 units of blood, 4 units of fresh frozen plasma and 5 units of platelets as well as 2 L of crystalloid and 4.5 L of colloid. In the evening her haemoglobin and clotting were normal. The value of having an epidural catheter was apparent when she needed a top-up of 5 mL of 0.5% bupivacaine, 30 min from the completion of surgery. From clinical experience of CSE, 5 mL of 0.5% bupivacaine should be given after 90 min and then 5 mL every 45 min. Our criteria for administering general anaesthesia for prolonged surgery with major haemorrhage are: 1. Hypotension causing unconsciousness. 2. A distressed patient who wishes to be asleep. 3. Inadequate anaesthesia. As the above case demonstrates, there is no need to administer general anaesthesia in major haemorrhage as long as the above criteria are met. A regional technique may, moreover, be beneficial, as being awake is the ultimate cerebral monitor. M. Garry R. Collis Anaesthetic Department, University Hospital of Wales, Cardiff, UK REFERENCES 1. Nanson J K, Sheikh A. Anaesthesia for emergency caesarean section in a parturient with bleeding placenta praevia and a potentially malignant hyperthermic-susceptible fetus.
doi: 10.1054/ijoa.2001.0838
Transposition of the great vessels: more experience I was interested to read the article by Yarrow and Russell on transposition of the great vessels in the June 2000 issue of IJOA.1 At the time I was involved in the care of a 29-year-old woman with surgically corrected transposition of the great vessels awaiting her fifth delivery. This woman has had more deliveries than any of those documented by Yarrow and Russell, and may therefore be of interest to others. The patient was born in 1970 and at 5 weeks of age her cyanotic spells were diagnosed as transposition of
251
the great vessels with patent ductus arteriosus. She initially had balloon septostomy and then closure of patent ductus arteriosus. In 1976 she had a Mustard atrial baffle repair. In 1981 she was admitted with rheumatic fever with carditis (fever, joint pain, raised ASO titre and changed murmur). She had subsequent admissions for ‘collapse’ associated with minor injuries, when she was noted to be bradycardic with a heart rate 38–40 bpm. It was considered that she might need a pacemaker in the future. In 1990 at the age of 19 years, she presented at another hospital for antenatal assessment in her first pregnancy. The case was reviewed by the cardiologist at 32 weeks’ gestation and she was noted to have a grade 2/6 midsystolic murmur over the sternum, and grade 2/6 blowing systolic murmur at the apex, with BP 125/80 mmHg. Her ECG showed sinus arrhythmia, right axis deviation and right ventricular hypertrophy. Chest Xray showed a cardiothoracic ratio of 55% and no evidence of congestive heart failure. She was admitted in spontaneous labour at 38 weeks’ gestation with preeclampsia, a diastolic pressure of 120 mmHg and 3+ proteinuria. Epidural analgesia was established with bupivacaine 0.5%, and two further top-ups were given. She was breathless and tachycardic during the second stage so the baby was delivered by elective outlet forceps. She remained hypertensive for 10 days post partum, and had evidence of congestive heart failure on day 6. She was eventually discharged home on day 13. She presented in her second pregnancy in 1992 with spontaneous onset of labour, and was admitted at 2 cm cervical dilatation. Epidural analgesia was established with bupivacaine 0.5% 10 mL, with one further top-up of bupivacaine 0.375% 8 mL. Outlet forceps delivery was carried out electively 8 h after admission. She had no post-partum complications and was discharged on day 5. In 1994, the patient was admitted to hospital after collapse at home. She had sepsis related to dental caries. Again she was noted to be bradycardic with heart rate of 40 bpm. In 1996 she had a miscarriage at 6 weeks. Preoperative ECG showed bradycardia of 38 bpm, right axis deviation and right ventricular hypertrophy as before. She first presented at our hospital in 1997. She was seen at antenatal clinic at 27 week’ gestation. She was admitted in spontaneous labour at 41 weeks’ gestation and epidural analgesia was established 2 h after admission, with bupivacaine 0.375% 10 mL plus fentanyl 50 µg, followed by infusion of bupivacaine 0.125% with fentanyl 2 µg/mL at 10 mL/h. She had a spontaneous vaginal delivery after 45 min in second stage. In her fifth pregnancy she was seen antenatally at 32 weeks’ gestation. She was admitted in spontaneous
252
International Journal of Obstetric Anesthesia
labour at 39 weeks’ gestation and 4 cm cervical dilatation. Epidural analgesia was requested but she reached full cervical dilatation and delivered spontaneously minutes later. She went home after 24 h. In her most recent pregnancy she was referred early to both anaesthetist (EL) and cardiologist. At 32 weeks she was noted to be tired with occasional palpitations but not short of breath. She had mild ankle oedema but no evidence of congestive heart failure. ECG showed sinus rhythm 66 bpm with occasional ectopic beats, and right ventricular hypertrophy. Her echocardiogram showed fractional shortening of right ventricle of 20%. At 38 weeks she was very tired with some breathlessness climbing stairs and hypotension (systolic 90 mmHg). Arrangements were made for close monitoring during labour, and early epidural analgesia. She was admitted in spontaneous labour at 40 weeks, transferred to the intensive care unit, and an epidural was placed 2 h later with ropivacaine 0.2% 10 mL and fentanyl 100 µg, followed by infusion of ropivacaine 0.2% at 6–8 mL/h. ECG, pulse oximetry and invasive blood pressure were monitored. She required Syntocinon infusion to augment labour, but had a rapid second stage of 12 min, and spontaneous vaginal delivery 7 h after admission. She showed no signs of heart failure. All deliveries and surgical interventions were covered with appropriate antibiotic prophylaxis and Syntocinon was given after each delivery. All her children are healthy. The patient has just had laparoscopic tubal ligation 6 weeks post partum, complicated by bradycardia to 28 bpm in the recovery period. E. Langton Department of Anaesthesia, Palmerston North Hospital, Palmerston North, New Zealand REFERENCE 1. Yarrow S, Russell R. Transposition of the great vessels: a series of three cases with a review of the literature. International Journal of Obstetric Anesthesia 2000; 9: 179–185.
doi: 10.1054/ijoa.2001.0839
CSE is the regional anaesthetic technique of choice for placenta praevia We read with interest the case report of a parturient with bleeding placenta praevia and a potentially malignant hyperthermia-susceptible fetus.1 We wonder why a combined spinal epidural (CSE) was not the method of anaesthesia chosen, as prolongation of surgery was a possibility and in a worse case scenario1 an obstetric hysterectomy might have been needed. In a review by Chestnut et al. of obstetric
hysterectomies,2 conversion to general anaesthesia was needed at 75 min in one case due to inadequate block. Also the mean operating time was over 2 h in his series of 46 patients. I appreciate that general anaesthesia could have been administered once the fetus was delivered but this is not an ideal situation. We recently performed a caesarean section on a patient with a grade 4 placenta praevia under CSE. After delivery there was major haemorrhage from the lower segment with a measured blood loss of 6 L in the space of an hour. A modified B-Lynch suture secured haemostasis. This required extensive uterine manipulation and exteriorisation. At no time was the patient hypotensive and she was happy to be awake throughout the procedure. At one stage while waiting for more blood (she had already had the 4 units crossmatched for her) we estimated that her haemoglobin was around 5 g/dL. Despite this she was co-operative and her husband remained with her throughout the procedure, both having been warned preoperatively about the possibility of major haemorrhage. Keeping her awake provided us with a valuable cerebral monitor, which would not have been available to us had she been asleep. In total she received 10 units of blood, 4 units of fresh frozen plasma and 5 units of platelets as well as 2 L of crystalloid and 4.5 L of colloid. In the evening her haemoglobin and clotting were normal. The value of having an epidural catheter was apparent when she needed a top-up of 5 mL of 0.5% bupivacaine, 30 min from the completion of surgery. From clinical experience of CSE, 5 mL of 0.5% bupivacaine should be given after 90 min and then 5 mL every 45 min. Our criteria for administering general anaesthesia for prolonged surgery with major haemorrhage are: 1. Hypotension causing unconsciousness. 2. A distressed patient who wishes to be asleep. 3. Inadequate anaesthesia. As the above case demonstrates, there is no need to administer general anaesthesia in major haemorrhage as long as the above criteria are met. A regional technique may, moreover, be beneficial, as being awake is the ultimate cerebral monitor. M. Garry R. Collis Anaesthetic Department, University Hospital of Wales, Cardiff, UK REFERENCES 1. Nanson J K, Sheikh A. Anaesthesia for emergency caesarean section in a parturient with bleeding placenta praevia and a potentially malignant hyperthermic-susceptible fetus.