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Correspondence Epidural infusion and neuropraxia
Epidural administration of saline was originally shown by Rice and Dabbs [I] to reduce the incidence of postdural puncture headache. Crawford, in 1972, reported a reduction in the incidence of such headache from 70% to 20% using 1-1.5 1 of saline over 24 h [2]. This success, together with the original study of epidural compliance [3], has led us to regard the epidural space as being fairly compliant, and which can tolerate such an infusion of saline without causing a significant rise in pressure. We wish to report a case of neuropraxia occuring during an epidural infusion which questions the safety of this practice. A 28-year-old, 70 kg, primiparous patient requested epidural analgesia during labour. The procedure was complicated by an accidental dural puncture at L,, with a 16 G Tuohy needle. An epidural catheter was subsequently sited at L2-, and used to provide analgesia for a forceps delivery. An epidural saline infusion was commenced at 20 ml.h-' and 9 h later the patient complained of severe back pain associated with paraesthesia and numbness in the distribution of L, to S,. Neurological examination failed to reveal any associated motor or autonomic abnormalities. The epidural infusion was immediately discontinued and the symptoms resolved over the next 3 h. A subsequent MRI scan was reported to illustrate narrowing of the spinal canal at the level of L,. This case illustrates that epidural compliance may be small and an infusion may then produce pressure effects and subsequent neuropraxia. The description of pain by the patient led us to stop the infusion; its continuation might have resulted in a more permanent neurological deficit. Pain on injection with any epidural procedure is an
important indication to cease injecting. It may represent an acute rise in epidural pressure or direct trauma, The practice of performing epidural saline infusions on a postoperative ward in the absence of an anaesthetist may result in delay in the termination of infusion if pain was to occur. If isotonic saline is to be used for the prophylaxis of postdural puncture headaches we would advocate the use of two bolus doses of 60 ml as an alternative to continuous infusion. This was first described by Craft in 1973 (41 and has the advantage that the anaesthetist is present throughout the duration of injection. This would allow one to terminate the injection at the first complaint of pain and thus limit any subsequent rise in pressure. University College Hospital, London W C l E 6 A U .
S.D. WOODS P. HODGSON T. WALKER D. HIGGINS
References [l] RICEGG, DABBS CH. The use of peridural and subarachnoid injections of saline solutions in the treatment of severe postspinal headache. Anesthesiology 1950; 11: 17-9. [2] CRAWFORD JS. The prevention of headache consequent upon dural puncture. British Journal of Anaesthesia 1972; 44: 598-600. [3] EVANSW. Intrasacral epidural injections in the treatment of sciatica. Lancer 1930; 2: 1225-7. [4] CRAFTJB, EPSTEIN BS, COAKLEY CS. Prophylaxis of dural puncture headache with epidural saline. Anesthesia and Analgesia 1973; 5 2 228-3 I .
Laparoscopy, surgical emphysema and ECG voltage A 52-year-old, 60 kg male, presented for laparoscopic cholecystectomy. His past medical history was not significant and pre-operative clinical, haematological, biochemical examinations and electrocardiogram were normal. Routine anaesthesia consisted of oral premedication with diazepam 10 mg and induction with etomidate 18 mg and fentanyl 0.2 mg. His trachea was intubated with a 9 mm cuffed orotracheal tube following suxamethonium 75 mg. His lungs were ventilated with NzO, O2 and enflurane 0.5%. Muscle relaxation was achieved with a bolus dose of atracurium 25 mg followed by an infusion of 25 mg.h-l. The Penlon Nuffield Ventilator (Anaesthesia Series 200) was used for intermittent positive pressure ventilation. Tidal volume was set at 600 ml, respiratory rate at 12 breath.min-'. Monitoring consisted of continuous display of the ECG, noninvasive blood pressure, capnography and pulse oximetry. As the surgeons had to explore the common bile duct, duration of the operation was about 4.5 h. Two hours after the start of the surgery, the ECG complexes were noticed to be of low voltage compared to those at the start of the operation and it was also noticed that both parotid regions of his neck and chest were
crepitant and swollen; surgical emphysema was diagnosed. The patient's peak inflation pressure remained the same, but oxygen saturation had decreased by 2-3% from 98-99%. The surgeons were informed and they immediately reduced the intra-abnormal pressure from 16 mmHg to 8 mmHg. As nitrous oxide might also have been contributing to the degree of cutaneous emphysema, it was decided to give 100% oxygen and anaesthesia maintained by increasing the enflurane concentration to 1.5% and introducing a propofol infusion 20-30 ml.h-'. Pneumothorax was not suspected on the basis of stable haemodynamics and oxygen saturation. During the next 2 h the subcutaneous emphysema decreased. Chest X ray at the end of surgery showed subcutaneous emphysema, pneunomediastinum, but no pneumothorax. Postoperative recovery was uneventful. This case illustrates that a diminution in ECG voltage, due to electrical insulation, could alert the anaesthetist of an ensuing surgical emphysema. Tung Wah Hospital, 12 Po Yan Street. ffong Kong
N. YOGASAKARAN
Anaesthesia for transvenous insertion of an automatic implantable cardioverter-defibrillator Carr and Whiteley state that the anaesthetic considerations for insertion of an automatic implantable cardioverterdefibrillator (AICD) as a formal surgical procedure are the same as for any major cardiac procedure (Anaesthesia 199I: 4 6 737-40). The anaesthetic implications of transvenous
insertion of an AICD may be different. The following case illustrates some of the problems associated with providing anaesthesia for transvenous insertion of an AICD. A 56-year-old, 80 kg male patient was scheduled for transvenous insertion of an AICD for repeated episodes of
Correspondence Epidural infusion and neuropraxia
Epidural administration of saline was originally shown by Rice and Dabbs [I] to reduce the incidence of postdural puncture headache. Crawford, in 1972, reported a reduction in the incidence of such headache from 70% to 20% using 1-1.5 1 of saline over 24 h [2]. This success, together with the original study of epidural compliance [3], has led us to regard the epidural space as being fairly compliant, and which can tolerate such an infusion of saline without causing a significant rise in pressure. We wish to report a case of neuropraxia occuring during an epidural infusion which questions the safety of this practice. A 28-year-old, 70 kg, primiparous patient requested epidural analgesia during labour. The procedure was complicated by an accidental dural puncture at L,, with a 16 G Tuohy needle. An epidural catheter was subsequently sited at L2-, and used to provide analgesia for a forceps delivery. An epidural saline infusion was commenced at 20 ml.h-' and 9 h later the patient complained of severe back pain associated with paraesthesia and numbness in the distribution of L, to S,. Neurological examination failed to reveal any associated motor or autonomic abnormalities. The epidural infusion was immediately discontinued and the symptoms resolved over the next 3 h. A subsequent MRI scan was reported to illustrate narrowing of the spinal canal at the level of L,. This case illustrates that epidural compliance may be small and an infusion may then produce pressure effects and subsequent neuropraxia. The description of pain by the patient led us to stop the infusion; its continuation might have resulted in a more permanent neurological deficit. Pain on injection with any epidural procedure is an
important indication to cease injecting. It may represent an acute rise in epidural pressure or direct trauma, The practice of performing epidural saline infusions on a postoperative ward in the absence of an anaesthetist may result in delay in the termination of infusion if pain was to occur. If isotonic saline is to be used for the prophylaxis of postdural puncture headaches we would advocate the use of two bolus doses of 60 ml as an alternative to continuous infusion. This was first described by Craft in 1973 (41 and has the advantage that the anaesthetist is present throughout the duration of injection. This would allow one to terminate the injection at the first complaint of pain and thus limit any subsequent rise in pressure. University College Hospital, London W C l E 6 A U .
S.D. WOODS P. HODGSON T. WALKER D. HIGGINS
References [l] RICEGG, DABBS CH. The use of peridural and subarachnoid injections of saline solutions in the treatment of severe postspinal headache. Anesthesiology 1950; 11: 17-9. [2] CRAWFORD JS. The prevention of headache consequent upon dural puncture. British Journal of Anaesthesia 1972; 44: 598-600. [3] EVANSW. Intrasacral epidural injections in the treatment of sciatica. Lancer 1930; 2: 1225-7. [4] CRAFTJB, EPSTEIN BS, COAKLEY CS. Prophylaxis of dural puncture headache with epidural saline. Anesthesia and Analgesia 1973; 5 2 228-3 I .
Laparoscopy, surgical emphysema and ECG voltage A 52-year-old, 60 kg male, presented for laparoscopic cholecystectomy. His past medical history was not significant and pre-operative clinical, haematological, biochemical examinations and electrocardiogram were normal. Routine anaesthesia consisted of oral premedication with diazepam 10 mg and induction with etomidate 18 mg and fentanyl 0.2 mg. His trachea was intubated with a 9 mm cuffed orotracheal tube following suxamethonium 75 mg. His lungs were ventilated with NzO, O2 and enflurane 0.5%. Muscle relaxation was achieved with a bolus dose of atracurium 25 mg followed by an infusion of 25 mg.h-l. The Penlon Nuffield Ventilator (Anaesthesia Series 200) was used for intermittent positive pressure ventilation. Tidal volume was set at 600 ml, respiratory rate at 12 breath.min-'. Monitoring consisted of continuous display of the ECG, noninvasive blood pressure, capnography and pulse oximetry. As the surgeons had to explore the common bile duct, duration of the operation was about 4.5 h. Two hours after the start of the surgery, the ECG complexes were noticed to be of low voltage compared to those at the start of the operation and it was also noticed that both parotid regions of his neck and chest were
crepitant and swollen; surgical emphysema was diagnosed. The patient's peak inflation pressure remained the same, but oxygen saturation had decreased by 2-3% from 98-99%. The surgeons were informed and they immediately reduced the intra-abnormal pressure from 16 mmHg to 8 mmHg. As nitrous oxide might also have been contributing to the degree of cutaneous emphysema, it was decided to give 100% oxygen and anaesthesia maintained by increasing the enflurane concentration to 1.5% and introducing a propofol infusion 20-30 ml.h-'. Pneumothorax was not suspected on the basis of stable haemodynamics and oxygen saturation. During the next 2 h the subcutaneous emphysema decreased. Chest X ray at the end of surgery showed subcutaneous emphysema, pneunomediastinum, but no pneumothorax. Postoperative recovery was uneventful. This case illustrates that a diminution in ECG voltage, due to electrical insulation, could alert the anaesthetist of an ensuing surgical emphysema. Tung Wah Hospital, 12 Po Yan Street. ffong Kong
N. YOGASAKARAN
Anaesthesia for transvenous insertion of an automatic implantable cardioverter-defibrillator Carr and Whiteley state that the anaesthetic considerations for insertion of an automatic implantable cardioverterdefibrillator (AICD) as a formal surgical procedure are the same as for any major cardiac procedure (Anaesthesia 199I: 4 6 737-40). The anaesthetic implications of transvenous
insertion of an AICD may be different. The following case illustrates some of the problems associated with providing anaesthesia for transvenous insertion of an AICD. A 56-year-old, 80 kg male patient was scheduled for transvenous insertion of an AICD for repeated episodes of
