British Journal of Anaesthesia 1992; 69: 422-425 CORRESPONDENCE
A. GUPTA M. VEGFOKS C. LBNNMARKEN
Linkoping 1. Fennelly ME, Powell H, Galledy DC, Whitwam JG. Midazolam sedation reversed with flumazenil for cardioversion. British Journal of Anaesthesia 1992; 68: 303-305. 2. Gupta A, Lennmarken C, Vegfors M, Tyden H. Anaesthesia for cardioversion: a comparison between propofol, thiopentone and midazolam. Anaesthesia 1990; 45: 872-875. 3. Krichbaum DW, Hamid I. Midazolam sedation and amnesia in elective cardioversion. Clinical Pharmacy 1988; 7: 423.
DELAYED SEPTICAEMIA AFTER EXTRADURAL STEROID TREATMENT Sir,—Further to the recent case report of a delayed complication after cxtradural steroid therapy [1], we wish to report a lifethreatening event associated with extradural steroid administration. A female of 54 yr was referred to the Pain Clinic for management of lower back pain which had been present for 9 months without improvement on conservative treatment. The pain radiated posteriorly to the left foot, was exacerbated by exercise and was restricting activity. The patient was generally well; she smoked 15 cigarettes per day, but denied respiratory symptoms. On examination, the single abnormal sign was limited straight leg raising on the left. Lumbar spine x-rays showed degenerative changes, particularly at the L4-5 region. A lumbar extradural injection of methyl prednisolone 120 mg (DepoMedrone) was performed using a strict aseptic technique. Nine days later, the patient began to notice a non-productive cough and became dyspnoeic; rigors developed and the following day she was admitted to hospital, where she was found to have pyrexia (temperature 39.9 °C), tachycardia and mild neck stiffness. Clinical signs of consolidation in the right chest were confirmed by chest x-ray. She became hypotensive (systolic arterial pressure 70 mm Hg) and required resuscitation with i.v. fluids. A diagnosis of septicaemia secondary to a chest infection was made. Investigations revealed haemoglobin 134 g litre"1, white blood cells 21.8 x 10* litre"1, with normal biochemistry; lumbar puncture was normal; blood and urine cultures subsequently were negative; no sputum could be obtained. I.v. cefuroxime and erythromycin therapy was initiated, the patient's condition improved rapidly and she was discharged home 6 days later. We consider that this patient's admission was precipitated by two factors: immunosuppression secondary to the steroid therapy
and cigarette smoking. Steroids have been administered by the extradural route for 40 yr [2] and the technique is considered to be safe in experienced hands. Local adverse effects, particularly haematoma [3], abscess [1,4] and bacterial meningitis [5], are well described, but systemic effects are often not considered and two major reviews of extradural steroid therapy discussed septicaemia without the presence of extradural abscess [6, 7]. Steroids depress the immune system via several routes [8]. Lymphopaenia affecting particularly the T helper cells occurs as the lymphocytes are sequestered into bone marrow; the resting macrophages are inhibited because of reduction in complement and IgG receptors; antigen handling by macrophages is impaired, leading to a poor primary antibody response; neutrophils fail to be exported into tissues. The effects of "depo" preparations can be shown to persist for up to 3 weeks [9]. We suggest therefore, that any patient receiving a depo preparation of steroid should be advised to seek medical advice at the earliest symptom of possible infection, and that medical staff should be aware of the possibility of late septicaemia. R. H. ELLIOTT B. J. COLLETT
Leicester 1. Sowter MC, Burgess NA, Woodsford PV, Lewis MH. Delayed presentation of an extradural abscess complicating thoracic extradural analgesia. British Journal of Anaesthesia 1992; 68: 103-105. 2. Robecchi A, Capra R. L'idrocortisone (composto F). Prime esperienze cliniche in campo reumatologico. Minerva Mcdica 1952; 2: 1259-1263. 3. Williams KN, Jackowski A, Evans PJD. Epidural haematoma requiring surgical decompression following repeated cervical epidural steroid injections for chronic pain. Pain 1990; 42: 197-199. 4. Shealy CM. Dangers of spinal injections without proper diagnosis. Journal of the American Medical Association 1966; 197: 1104-1106. 5. Dougherty JH, Frazer RA. Complications following intraspinal injections of steroids. Journal of Neurosurgery 1978; 48: 1023-1025. 6. Kepes ER, Duncalf D. Treatment of backache with spinal injections of local anesthetics, spinal and systemic steroids. A review. Pain 1985; 22: 33-37. 7. Benzon HT. Epidural steroid injections for low back pain and lumbosacral radiculopathy. Pain 1986; 24: 277-295. 8. Chapel H, Haeney M. Essentials of Clinical Immunology, 2nd Edn. Oxford: Blackwell Scientific Publications, 1988; 135136. 9. Bum JM, Langdon L. Duration of action of methyl prednisolone. A study in patients with the lumbosciatic syndrome. American Journal of Physical Medicine 1974; S3: 29-34.
Sir,-We are grateful for the opportunity to comment on the letter of Elliott and Collett, in response to our report [1]. They report a case of septicaemia following extradural administration of steroids for the relief of back pain which is not comparable to our own. Ours was a thoracic administration, analgesics were administered and our patient developed a local septic complication. We would, however, take issue with the authors. We would agree that smoking was a factor in the development of a chest infection in their patient, but dispute the importance of the extradural steroids. The small dose of methyl prednisolone administered (120 mg) into the extradural space would seem unlikely to be sufficient to cause generalized immunosuppression. Certainly, it is much smaller than that administered i.v. for therapeutic immunosuppression. In contrast, our patient was immunosuppressed by rheumatoid arthritis and the administration of long-term high-dose immunosuppressive drugs. This is seen in the white cell response to infection — 6.8 x 10* litre"1 in our patient, but 21.8 x 10* litre""1 in theirs.
Downloaded from http://bja.oxfordjournals.org/ at RMIT University Library on July 25, 2015
MIDAZOLAM AND CARDIOVERSION Sir,—We read with interest the article by Fennelly and others [1], and wish to report our own experience, which is different in some respects. The main difference between their study and ours [2] was that the dose of midazolam we used was much greater in order to induce anaesthesia (and not sedation). Although benzodiazepines are known to cause anterograde amnesia, Krichbaum and Hamid [3] reported a few patients who were aware during cardioversion under midazolam sedation. Our own experience was that the anaesthesia produced by midazolam, in a much greater dose, was poor because many patients had flexion movements of the arms and legs and some needed to be restrained. Flumazenil clearly reversed the effect of midazolam, but many patients were resedated at the time of interview 4 h later. Also, the statement that this was "the first specific report of the use of midazolam, reversed by flumazenil, for anaesthesia for cardioversion" is incorrect, as both the above studies [2,3] have examined midazolam sedation for cardioversion. Although the purpose of the present study was not to evaluate the usefulness of midazolam as an anaesthetic for cardioversion, we think that it is important for the reader to know that midazolam is not the best choice for this procedure, even though it can be reversed effectively by flumazenil.
423
CORRESPONDENCE In summary, therefore, we welcome the interest shown by Elliott and Collett, but feel that their patient suffered as a consequence of smoking, rather than of their intervention. M. W. SCRIVEN N. A. BURGESS P. W . WOODSFORD M. H. LEWIS Glamorgan
1. Sowter MC, Burgess NA, Woodsford PV, Lewis MH. Delayed presentation of an enradural abscess complicating thoracic extradural analgesia. British Journal of Anaesthesia 1992; 68: 103-105. STEROID THERAPY AND EXTRADURAL ANALGESIA Sir,—I read with interest the case report of Dr Sowter and colleagues [1] describing the delayed presentation of an extradural abscess in a patient with rheumatoid arthritis who had been receiving steroids, and the letter by McQuay and Jadad [2] who have criticized as premature the suggestion that extradural techniques should be contraindicated in such patients. McQuay and Jadad base their criticism on the observation that this is but a single case; furthermore, they comment that there have been no cases of delayed extradural abscess in patients receiving steroids by the extradural route for the management of chronic back pain and that there have been no reports of extradural abscesses in cancer patients taking oral steroids who receive extradural therapy. In fact there have been reports of extradural abscesses occurring after administration of extradural steroids for back pain and an extradural abscess has occurred in a patient who was taking oral steroids but did not have cancer. Chan and Leung [3] described a diabetic patient who developed an extradural abscess after a single extradural injection of triamcinolone acetonide for sciatica. Similarly, Goucke and Graziorti [4] described a patient who developed an extradural abscess 3 weeks after receiving a course of three extradural injections of methylprednisolone and local anaesthetic for chronic back pain. Strong [5] described delayed presentation of an extradural abscess after placement of extradural catheters in two patients who received steroids; the first patient suffered from herpes zoster and received extradural methylprednisolone, the second patient suffered from reflex sympathetic dystrophy and had been receiving oral prednisone. McQuay and Jadad also refer to a case of an iatrogenic extradural abscess that occurred in a patient 9 days after removal of an extradural catheter, suggesting Dr Sowter's paper to be the third report of extradural abscess with delayed presentation. In fact there have been several other reports of iatrogenic extradural abscesses with delayed presentation which have occurred up to 5 months after placement of extradural catheters [5-7], It is debatable if concurrent steroid use should be a contraindication to extradural therapy. However, it seems prudent to urge caution whenever a patient is receiving steroids or when steroids are to be administered extradurally. The risk and benefit must be considered, informed consent obtained, scrupulous attention given to aseptic technique, and the patient must be carefully followed up to check for signs of complications.
hematoma and spinal abscess following peridural anesthesia. Regional Anesthesie 1987; 10: 121-124.
7. Reynolds PC, Hahn MB. Early diagnosis of a spinal epidural abscess. Regional Anesthesia 1991; 16: 47-58. INSULATED REGIONAL BLOCK NEEDLES Sir,—As a regular user of insulated needles, I was very interested to read the article by Jones, De Jonge and Smith [1] on the use of uninsulated needles in local anaesthetic blocks. However, one of the basic premises of their article seems to be at odds with general perceptions. • I refer to the unreferenced statements that "the form... of the voltage field surrounding the needle... is important", and "the nerve is most likely to be stimulated when it lies within a steep voltage gradient." In support of this they stated that a reduction of the transmembrane potential to a value of 55 mV generates a spike potential, and that this can be achieved by movement of ions caused by a potential gradient in the area of the nerve. It is not immediately obvious to me how a movement of ions per se (i.e. current) would reduce the transmembrane potential. A major factor in the determination of the transmembrane potential is, however, the absolute voltage surrounding the nerve, and it may be this, rather than its gradient, that is the important measure. Indeed, in a previous work on the subject, Bashein, Haschke and Ready [2] referred to zones of depolarization with reference to their potential, rather than to their potential gradient. The fact that stimulation of a nerve is more reproducible with a given current through the needle than with a given potential difference between it and the earth electrode may be explained by the fact that there is a variable resistance in the area of the earth electrode itself. If the needle is embedded in extracellular fluid, the resistance characteristics around it are unlikely to vary much between sites or even between patients: extracellular fluid has a constant composition. (The search for nerves embedded in fat may be a different matter.) Achieving a constant current would therefore produce a constant pattern of potentials around the needle. Development of this line of reasoning would refute the conclusions of Jones, De Jonge and Smith that an insulated needle would be as likely to fire a spike potential in a nerve that lay significantly in front of or behind the tip as it would be if the tip were adjacent to the nerve, and that in the case of an uninsulated needle, stimulation would occur only if the needle (I presume they mean the tip of the needle) is within 2 mm of the nerve. I agree that the steep diminution of potential in front of an insulated needle results in a more accurate localization of the nerve as the needle approaches it, but I suggest that this would be offset by a lower accuracy of localization when the needle has been advanced so that the nerve lies to the side of the needle. M. S. READ
Montpellier
Wellington, New Zealand •
1. Jones RP, De Jonge M, Smith BE. Voltage fields surrounding needles used in regional anaesthesia. British Journal of Anaesthesia 1992; 68: 515-518. 2. Bashein G, Haschke RH, Ready LB. Electrical nerve location: numerical and electrophoretic comparison of insulated vs uninsulated needles. Anesthesia and Analgesia 1984; 63: 919-924.
1. Sowter MC, Burgess NA, Woodsford PV, Lewis MH. Delayed presentation of an extradural abscess complicating thoracic extradural analgesia. British Journal of Anaesthesia 1992; 68: 103-105. 2. McQuay HJ, Jadad AR. Is steroid therapy a contraindication to extradural analgesia? British Journal of Anaesthesia 1992; 68:540-541. 3. Chan ST, Leung S. Spinal epidural abscess following steroid injection for sciatica. Spine 1989; 14: 106-108. 4. Goucke CR, Graziotti P. Extradural jibscess following local -anaestheticand steroid injection for chronic back pain. British Journal of Anaesthesia 1990; 65: 427^429. 5. Strong WE. Epidural abscess associated with epidural catheterization: A rare event? Report of two cases with markedly delayed presentation. Ancsthesiology 1991; 74: 943-946. 6. Sollmann WP, Gaab MR, Panning B. Lumbar epidural
Sir,—We are grateful for the opportunity to respond to the letter from Dr Read, and agree with the final summarizing statement. We feel that such conclusions confirm the statement of Pither, Raj and Ford that "while both types of needle have their advocates, knowledge of their electrical behaviour enables both to be used effectively" [1]. However, we are at a variance with the reasoning that leads to the final statement. On the basis of the_electrophysiology-of nerve conduction~[2], we believe that it is the voltage gradient across the nerve membrane (transmembrane potential) that determines the conduction state of a nerve. " Zones of depolarization " is a term used by Bashein, Haschke and Ready [3], but the term is not defined clearly and the plots used in their computer simulation represent contours of constant field magnitude based on mathematical models in communication electronics. In our experimental model, we attempted to create conditions that were more
W. D. NGAN KEE
A. GUPTA M. VEGFOKS C. LBNNMARKEN
Linkoping 1. Fennelly ME, Powell H, Galledy DC, Whitwam JG. Midazolam sedation reversed with flumazenil for cardioversion. British Journal of Anaesthesia 1992; 68: 303-305. 2. Gupta A, Lennmarken C, Vegfors M, Tyden H. Anaesthesia for cardioversion: a comparison between propofol, thiopentone and midazolam. Anaesthesia 1990; 45: 872-875. 3. Krichbaum DW, Hamid I. Midazolam sedation and amnesia in elective cardioversion. Clinical Pharmacy 1988; 7: 423.
DELAYED SEPTICAEMIA AFTER EXTRADURAL STEROID TREATMENT Sir,—Further to the recent case report of a delayed complication after cxtradural steroid therapy [1], we wish to report a lifethreatening event associated with extradural steroid administration. A female of 54 yr was referred to the Pain Clinic for management of lower back pain which had been present for 9 months without improvement on conservative treatment. The pain radiated posteriorly to the left foot, was exacerbated by exercise and was restricting activity. The patient was generally well; she smoked 15 cigarettes per day, but denied respiratory symptoms. On examination, the single abnormal sign was limited straight leg raising on the left. Lumbar spine x-rays showed degenerative changes, particularly at the L4-5 region. A lumbar extradural injection of methyl prednisolone 120 mg (DepoMedrone) was performed using a strict aseptic technique. Nine days later, the patient began to notice a non-productive cough and became dyspnoeic; rigors developed and the following day she was admitted to hospital, where she was found to have pyrexia (temperature 39.9 °C), tachycardia and mild neck stiffness. Clinical signs of consolidation in the right chest were confirmed by chest x-ray. She became hypotensive (systolic arterial pressure 70 mm Hg) and required resuscitation with i.v. fluids. A diagnosis of septicaemia secondary to a chest infection was made. Investigations revealed haemoglobin 134 g litre"1, white blood cells 21.8 x 10* litre"1, with normal biochemistry; lumbar puncture was normal; blood and urine cultures subsequently were negative; no sputum could be obtained. I.v. cefuroxime and erythromycin therapy was initiated, the patient's condition improved rapidly and she was discharged home 6 days later. We consider that this patient's admission was precipitated by two factors: immunosuppression secondary to the steroid therapy
and cigarette smoking. Steroids have been administered by the extradural route for 40 yr [2] and the technique is considered to be safe in experienced hands. Local adverse effects, particularly haematoma [3], abscess [1,4] and bacterial meningitis [5], are well described, but systemic effects are often not considered and two major reviews of extradural steroid therapy discussed septicaemia without the presence of extradural abscess [6, 7]. Steroids depress the immune system via several routes [8]. Lymphopaenia affecting particularly the T helper cells occurs as the lymphocytes are sequestered into bone marrow; the resting macrophages are inhibited because of reduction in complement and IgG receptors; antigen handling by macrophages is impaired, leading to a poor primary antibody response; neutrophils fail to be exported into tissues. The effects of "depo" preparations can be shown to persist for up to 3 weeks [9]. We suggest therefore, that any patient receiving a depo preparation of steroid should be advised to seek medical advice at the earliest symptom of possible infection, and that medical staff should be aware of the possibility of late septicaemia. R. H. ELLIOTT B. J. COLLETT
Leicester 1. Sowter MC, Burgess NA, Woodsford PV, Lewis MH. Delayed presentation of an extradural abscess complicating thoracic extradural analgesia. British Journal of Anaesthesia 1992; 68: 103-105. 2. Robecchi A, Capra R. L'idrocortisone (composto F). Prime esperienze cliniche in campo reumatologico. Minerva Mcdica 1952; 2: 1259-1263. 3. Williams KN, Jackowski A, Evans PJD. Epidural haematoma requiring surgical decompression following repeated cervical epidural steroid injections for chronic pain. Pain 1990; 42: 197-199. 4. Shealy CM. Dangers of spinal injections without proper diagnosis. Journal of the American Medical Association 1966; 197: 1104-1106. 5. Dougherty JH, Frazer RA. Complications following intraspinal injections of steroids. Journal of Neurosurgery 1978; 48: 1023-1025. 6. Kepes ER, Duncalf D. Treatment of backache with spinal injections of local anesthetics, spinal and systemic steroids. A review. Pain 1985; 22: 33-37. 7. Benzon HT. Epidural steroid injections for low back pain and lumbosacral radiculopathy. Pain 1986; 24: 277-295. 8. Chapel H, Haeney M. Essentials of Clinical Immunology, 2nd Edn. Oxford: Blackwell Scientific Publications, 1988; 135136. 9. Bum JM, Langdon L. Duration of action of methyl prednisolone. A study in patients with the lumbosciatic syndrome. American Journal of Physical Medicine 1974; S3: 29-34.
Sir,-We are grateful for the opportunity to comment on the letter of Elliott and Collett, in response to our report [1]. They report a case of septicaemia following extradural administration of steroids for the relief of back pain which is not comparable to our own. Ours was a thoracic administration, analgesics were administered and our patient developed a local septic complication. We would, however, take issue with the authors. We would agree that smoking was a factor in the development of a chest infection in their patient, but dispute the importance of the extradural steroids. The small dose of methyl prednisolone administered (120 mg) into the extradural space would seem unlikely to be sufficient to cause generalized immunosuppression. Certainly, it is much smaller than that administered i.v. for therapeutic immunosuppression. In contrast, our patient was immunosuppressed by rheumatoid arthritis and the administration of long-term high-dose immunosuppressive drugs. This is seen in the white cell response to infection — 6.8 x 10* litre"1 in our patient, but 21.8 x 10* litre""1 in theirs.
Downloaded from http://bja.oxfordjournals.org/ at RMIT University Library on July 25, 2015
MIDAZOLAM AND CARDIOVERSION Sir,—We read with interest the article by Fennelly and others [1], and wish to report our own experience, which is different in some respects. The main difference between their study and ours [2] was that the dose of midazolam we used was much greater in order to induce anaesthesia (and not sedation). Although benzodiazepines are known to cause anterograde amnesia, Krichbaum and Hamid [3] reported a few patients who were aware during cardioversion under midazolam sedation. Our own experience was that the anaesthesia produced by midazolam, in a much greater dose, was poor because many patients had flexion movements of the arms and legs and some needed to be restrained. Flumazenil clearly reversed the effect of midazolam, but many patients were resedated at the time of interview 4 h later. Also, the statement that this was "the first specific report of the use of midazolam, reversed by flumazenil, for anaesthesia for cardioversion" is incorrect, as both the above studies [2,3] have examined midazolam sedation for cardioversion. Although the purpose of the present study was not to evaluate the usefulness of midazolam as an anaesthetic for cardioversion, we think that it is important for the reader to know that midazolam is not the best choice for this procedure, even though it can be reversed effectively by flumazenil.
423
CORRESPONDENCE In summary, therefore, we welcome the interest shown by Elliott and Collett, but feel that their patient suffered as a consequence of smoking, rather than of their intervention. M. W. SCRIVEN N. A. BURGESS P. W . WOODSFORD M. H. LEWIS Glamorgan
1. Sowter MC, Burgess NA, Woodsford PV, Lewis MH. Delayed presentation of an enradural abscess complicating thoracic extradural analgesia. British Journal of Anaesthesia 1992; 68: 103-105. STEROID THERAPY AND EXTRADURAL ANALGESIA Sir,—I read with interest the case report of Dr Sowter and colleagues [1] describing the delayed presentation of an extradural abscess in a patient with rheumatoid arthritis who had been receiving steroids, and the letter by McQuay and Jadad [2] who have criticized as premature the suggestion that extradural techniques should be contraindicated in such patients. McQuay and Jadad base their criticism on the observation that this is but a single case; furthermore, they comment that there have been no cases of delayed extradural abscess in patients receiving steroids by the extradural route for the management of chronic back pain and that there have been no reports of extradural abscesses in cancer patients taking oral steroids who receive extradural therapy. In fact there have been reports of extradural abscesses occurring after administration of extradural steroids for back pain and an extradural abscess has occurred in a patient who was taking oral steroids but did not have cancer. Chan and Leung [3] described a diabetic patient who developed an extradural abscess after a single extradural injection of triamcinolone acetonide for sciatica. Similarly, Goucke and Graziorti [4] described a patient who developed an extradural abscess 3 weeks after receiving a course of three extradural injections of methylprednisolone and local anaesthetic for chronic back pain. Strong [5] described delayed presentation of an extradural abscess after placement of extradural catheters in two patients who received steroids; the first patient suffered from herpes zoster and received extradural methylprednisolone, the second patient suffered from reflex sympathetic dystrophy and had been receiving oral prednisone. McQuay and Jadad also refer to a case of an iatrogenic extradural abscess that occurred in a patient 9 days after removal of an extradural catheter, suggesting Dr Sowter's paper to be the third report of extradural abscess with delayed presentation. In fact there have been several other reports of iatrogenic extradural abscesses with delayed presentation which have occurred up to 5 months after placement of extradural catheters [5-7], It is debatable if concurrent steroid use should be a contraindication to extradural therapy. However, it seems prudent to urge caution whenever a patient is receiving steroids or when steroids are to be administered extradurally. The risk and benefit must be considered, informed consent obtained, scrupulous attention given to aseptic technique, and the patient must be carefully followed up to check for signs of complications.
hematoma and spinal abscess following peridural anesthesia. Regional Anesthesie 1987; 10: 121-124.
7. Reynolds PC, Hahn MB. Early diagnosis of a spinal epidural abscess. Regional Anesthesia 1991; 16: 47-58. INSULATED REGIONAL BLOCK NEEDLES Sir,—As a regular user of insulated needles, I was very interested to read the article by Jones, De Jonge and Smith [1] on the use of uninsulated needles in local anaesthetic blocks. However, one of the basic premises of their article seems to be at odds with general perceptions. • I refer to the unreferenced statements that "the form... of the voltage field surrounding the needle... is important", and "the nerve is most likely to be stimulated when it lies within a steep voltage gradient." In support of this they stated that a reduction of the transmembrane potential to a value of 55 mV generates a spike potential, and that this can be achieved by movement of ions caused by a potential gradient in the area of the nerve. It is not immediately obvious to me how a movement of ions per se (i.e. current) would reduce the transmembrane potential. A major factor in the determination of the transmembrane potential is, however, the absolute voltage surrounding the nerve, and it may be this, rather than its gradient, that is the important measure. Indeed, in a previous work on the subject, Bashein, Haschke and Ready [2] referred to zones of depolarization with reference to their potential, rather than to their potential gradient. The fact that stimulation of a nerve is more reproducible with a given current through the needle than with a given potential difference between it and the earth electrode may be explained by the fact that there is a variable resistance in the area of the earth electrode itself. If the needle is embedded in extracellular fluid, the resistance characteristics around it are unlikely to vary much between sites or even between patients: extracellular fluid has a constant composition. (The search for nerves embedded in fat may be a different matter.) Achieving a constant current would therefore produce a constant pattern of potentials around the needle. Development of this line of reasoning would refute the conclusions of Jones, De Jonge and Smith that an insulated needle would be as likely to fire a spike potential in a nerve that lay significantly in front of or behind the tip as it would be if the tip were adjacent to the nerve, and that in the case of an uninsulated needle, stimulation would occur only if the needle (I presume they mean the tip of the needle) is within 2 mm of the nerve. I agree that the steep diminution of potential in front of an insulated needle results in a more accurate localization of the nerve as the needle approaches it, but I suggest that this would be offset by a lower accuracy of localization when the needle has been advanced so that the nerve lies to the side of the needle. M. S. READ
Montpellier
Wellington, New Zealand •
1. Jones RP, De Jonge M, Smith BE. Voltage fields surrounding needles used in regional anaesthesia. British Journal of Anaesthesia 1992; 68: 515-518. 2. Bashein G, Haschke RH, Ready LB. Electrical nerve location: numerical and electrophoretic comparison of insulated vs uninsulated needles. Anesthesia and Analgesia 1984; 63: 919-924.
1. Sowter MC, Burgess NA, Woodsford PV, Lewis MH. Delayed presentation of an extradural abscess complicating thoracic extradural analgesia. British Journal of Anaesthesia 1992; 68: 103-105. 2. McQuay HJ, Jadad AR. Is steroid therapy a contraindication to extradural analgesia? British Journal of Anaesthesia 1992; 68:540-541. 3. Chan ST, Leung S. Spinal epidural abscess following steroid injection for sciatica. Spine 1989; 14: 106-108. 4. Goucke CR, Graziotti P. Extradural jibscess following local -anaestheticand steroid injection for chronic back pain. British Journal of Anaesthesia 1990; 65: 427^429. 5. Strong WE. Epidural abscess associated with epidural catheterization: A rare event? Report of two cases with markedly delayed presentation. Ancsthesiology 1991; 74: 943-946. 6. Sollmann WP, Gaab MR, Panning B. Lumbar epidural
Sir,—We are grateful for the opportunity to respond to the letter from Dr Read, and agree with the final summarizing statement. We feel that such conclusions confirm the statement of Pither, Raj and Ford that "while both types of needle have their advocates, knowledge of their electrical behaviour enables both to be used effectively" [1]. However, we are at a variance with the reasoning that leads to the final statement. On the basis of the_electrophysiology-of nerve conduction~[2], we believe that it is the voltage gradient across the nerve membrane (transmembrane potential) that determines the conduction state of a nerve. " Zones of depolarization " is a term used by Bashein, Haschke and Ready [3], but the term is not defined clearly and the plots used in their computer simulation represent contours of constant field magnitude based on mathematical models in communication electronics. In our experimental model, we attempted to create conditions that were more
W. D. NGAN KEE
