327
CORRESPONDENCE
Sir,—I am grateful for the comments of Drs Seex and Eldridge on my review of management of hyponatraemia. In the study reported by Nelson and colleagues [1], 10 of 12 patients with intracranial disease had hyponatraemia associated with plasma volume correction, whilst in the remaining two patients plasma volume was expanded, suggesting ADH-induced water retention. However, even where evidence for volume contraction could be demonstrated, free water clearance was clearly impaired, as the normal physiological response to a reduction in serum sodium would be an increase in free water clearance and correction of dilutional hyponatraemia. The mechanism for reduced free water clearance is probably ADH release in response to extracellular volume contraction, rather than increased extracellular tonicity [2], although local renal mechanisms may also play a role [3]. It seems likely, therefore, that hyponatraemia secondary to cerebral salt wasting reflects an appropriate physiological response to extracellular fluid volume contraction (table I in my review), rather than inappropriate secretion of ADH. Hyponatraemia in this situation, therefore, does not differ from that observed in any condition characterized by sodium depletion. However, the important point raised still stands. Where there is unequivocal evidence of extracellular fluid volume contraction, the correct therapy is repletion rather than water restriction. It should be borne in mind that hyponatraemia in some patients with cerebral disease may also be attributable to inappropriate ADH secretion [1,4]. In this situation water restriction is the first appropriate therapy. It is important to distinguish, therefore, between these two quite different clinical situations, both of which result in hyponatraemia. J. D. SWALES
Leicester REFERENCES 1. Nelson PB, Seif SM, Maroon JC, Robinson AG. Hyponatraemia in intracranial disease: perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Journal of Neurosurgery 1981; 55: 938-941. 2. Leaf A, Mamby AR. Antidiuretic mechanism not regulated by extracellular tonicity. Journal of Clinical Investigation 1952; 31: 60-71. 3. Harrington AR. Hyponatremia due to sodium depletion in the absence of vasopressin. American Journal of Physiology 1972; 222: 768-774. 4. Haden HT, Knox GW. Cerebral hyponatremia with inappropriate antidiuretic hormone syndrome. American Journal of Medical Science 1965; 249: 381-390.
" NEEDLE-THROUGH-NEEDLE " TECHNIQUE FOR COMBINED SPINAL-EXTRADURAL ANAESTHESIA IN OBSTETRICS Sir,—We were interested to read recent correspondence concerning combined spinal-extradural anaesthesia in obstetrics [1,2]. At Queen Charlotte's and Chelsea Hospital, we use the necdle-through-needle technique preferentially and arc currently evaluating various aspects with a prospective trial. We agree with Dr Kestin that placing the patient in a lateral position is to be favoured, to minimize the effects of hypotension, and with Dr Brownridge that the mothers need complete attention after the subarachnoid injection. If the extradural catheter fails to thread after the spinal injection, we abandon insertion attempts and turn the mother as soon as possible onto her other side to produce a bilateral block. We consider a unilateral block to be a failure. We then commence an infusion of ephedrine to avoid hypotension [3] and then we insert an extxadural catheter without hurry. This does not lead to significant delay starting surgery, and avoids the uncertainty of dose requirements in the extradural space having to be superimposed on a poor subarachnoid block. Less clear to us, though, is the difficulty of testing the position of the extradural catheter placed after the spinal has been performed and it is this matter in particular that we feel needs to be addressed. To protect the mother against the problems of accidental i.v. injection, the top-ups we give contain 0.5% bupivacaine with 1 in 200000 adrenaline and 2% lignocaine in equal proportions. Use of lignocaine has been suggested to diminish the cardiotoxicity of bupivacaine [4]. The adrenaline may produce tachycardia if given i.v., although this is questioned [5]. We feel the needle-through-needle technique has an important place in obstetric practice, for both routine and emergency situations [6]. It appears to us that the problems are fairly minor and the advantages of speed, efficacy and flexibility are wholly desirable in an emergency. M. J. G. FAMILTON B. M. MORGAN
London
1. 2. 3. 4. 5. 6.
REFERENCES Brownridge P. Spinal anaesthesia in obstetrics. British Journal of Anaesthesia 1991; 67: 663. Kestin IG. Spinal anaesthesia in obstetrics. British Journal of Anaesthesia 1991; 67: 663. Kang YG, Abouleish E, Caritis S. Prophylactic intravenous ephedrine infusion during spinal anesthesia for Cesarean anesthesia. Anesthesia and Analgesia 1982; 62: 839-842. De Jong RN, Bonin JD. Mixtures of local anesthetics arc no more toxic than parent drugs. Anesthesiology 1989; 54: 177-181. Leighton BL, Norris MC. The test dose revisited again. Anesthesiology 1988; 68: 87. Carrie LES. Extradural, spinal or combined block for obstetric surgical anaesthesia. British Journal of Anaesthesia 1990; 65: 225-223.
"NEUROLOGICAL" COMPLICATIONS OF EXTRADURAL BUPIVACAINE Sir,—Drs Dunne and Kox [1] describe a patient with a combination of respiratory and cerebral signs after a road traffic accident. The cerebral signs are ascribed to a systemic reaction to an extradural infusion of bupivacaine given for pain relief. I would suggest that the most likely cause of the features seen in this patient was a fat embolism syndrome—a diagnosis that must always be kept in mind when a patient develops signs of cerebral irritation after orthopaedic trauma, and a diagnosis made usually by exclusion. I must indicate, therefore, why I would exclude bupivacaine as the primary cause of the problem. First, the clinical features of the reaction were not those associated with systemic toxicity to local anaesthetic drugs, although I accept that the response to chronic administration may not be the same as in the acute, "accidental" situation. Second, the authors refer to the "rapid clearance" of bupivacaine in their patient after the infusion was stopped, yet note that it took more
Downloaded from http://bja.oxfordjournals.org/ at University of Leeds on May 17, 2015
3. Schwartz WB, Bennett W, Curelop S, Bamer FC. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. American Journal of Medicine 1957; 23: 529-542. 4. Nelson PB, Seif SM, Maroon JC, Robinson AG. Hyponatremia in intracranial disease: perhaps not the syndrome of innappropriate secretion of antidiuretic hormone (SIADH). Journal of Neurosurgery 1981; 55: 938-941. 5. Rosenfeld JV, Barnett GH, Sila CA, Little JR, Bravo EL, Beck GJ. The effect of subarachnoid hemorrhage on blood and CSF atrial natriuretic factor. Journal of Neurontrgery 1989; 71: 32-37. 6. Weinand ME, O'Boynick PL, Goetz KL. A study of serum anridiuretic hormone and atrial natriuretic peptide levels in a series of patients with intracranial disease and hyponatremia. Neurosurgery 1989; 25: 781-785. 7. Fox, JL, Falik JL, Shaloub RJ. Neurosurgical hyponatremia. The role of antidiuresis. Journal of Neurosurgery 1971; 34: 506-514. 8. Lolin Y, Jackowski A, Symon L. Disordered salt and water regulation in neurosurgical practice: modern managment perspectives. Journal of Neurology, Neurosurgery and Psychiatry 1991: (in press). 9. Wijdicks EFM, Vermeulen M, Hijdra A, van Gijn J. Hyponatracmia and cerebral infarction in patients with ruptured intracranial aneurysms. Is fluid restriction harmful? Annals of Neurology 1985; 17: 137-140.
BRITISH JOURNAL OF ANAESTHESIA
328 than 72 h for the clinical condition to resolve. Third, the peak concentration measured (4 mg litre"1) is large, but is noted not infrequently in kinetic studies of regional anaesthesia with bupivacaine, with unremarkable effects. In this regard, the authors may have been led astray by the opinion they received on plasma concentrations from the New Cross Poisons Unit. To indicate that plasma concentrations of bupivacaine should not exceed 1 mg litre"1 is, I am afraid, a pronouncement without foundation. J. A. W. WlLDSMITH Edinburgh
REFERENCE 1. Dunne NM, Kox WJ. Neurological complications following the use of continuous extradural analgesia with bupivacaine. British Journal of Anaesthesia 1991; 66: 617-619.
3 ml and adrenaline 15 ng was not very sensitive for detecting intravascular injection, as moderate or false negative responses occurred frequently" [1]. Should this prohibit them from administering a test dose on the basis that "...atropine 0.5 mg is used routinely in our institution before extradural block is performed, in order to prevent bradycardia"? [1]. Why not: 1) administer the test dose; 2) take the time (2 min) to evaluate it; 3) give 0.5 mg of atropine i.v.; and 4) then immediately follow it with the therapeutic dose of the local anaesthetic ? Doing so would still give i.v. atropine 5 min to suppress "vagal bradycardia". When a therapeutic dose of a local anaesthetic is injected into the lumbar area of the extradural space, it seldom results in a bradycardia until 5 min or more elapses. Therefore, would not administration of atropine in the suggested sequence allow "the best of two worlds", namely, ruling out the possibility of a systemic toxic reaction or a total spinal anaesthetic by the test dose and avoiding a vagal bradycardia by i.v. atropine? D. C. MOORE
G. JONES M. LOGAN Edinburgh
REFERENCES 1. Dunne NM, Kox WJ. Neurological complications following the use of continuous cxtradural analgesia with bupivacaine. British Journal of Anaesthesia 1991; 66: 617-619. 2. Scott DB, Lee A, Fagan D, Bowler GMR, Bloomfield P, Lundh R. Acute toxicity of ropivacaine compared with that of bupivacaine. Anesthesia and Analgesia 1989; 69: 563-569.
ATROPINE AND THE TEST DOSE Sir,—Narchi and colleagues stated: "To be useful, a test dose must be both specific and sensitive. The lack of specificity has already been demonstrated in parturients who exhibited false positive responses to an adrenaline test dose (increases in HR [heart rate] after injection of bupivacaine without adrenaline)" [1]. To support this statement, they cited Cartwright, McCarrol and Antzaka [2]. Evidently they were unaware that the validity of that study was questionable. Its methodology was based on 3 ml of solution being injected through plastic tubing (catheter) at 1 ml s"1, which is impossible [3]. As to sensitivity, Narchi and colleagues found that atropine 0.5 mg i.v. 5 min before "a test dose containing 2% lignocaine
Seattle REFERENCES 1. Narchi P, Mazoit JX, Cohen S, Samii K. Heart rate response to an i.v. test dose of adrenaline and lignocaine with and without atropine pretrcatment. British Journal of Anaesthesia 1991; 66: 583-586. 2. Cartwright PD, McCarrol SM, Antzaka C. Maternal heart rate changes with a plain epidural test dose. Anesthesiology 1986; 65: 226-228. 3. Moore DC, Batra MS, Bridenbaugh LD, Brown DL, Carpenter RL, Hecker BR, Ramsey D. Maternal heart rate changes with a plain epidural test dose—validity of results open to question. Anesthesiology 1987; 66: 854. Sir,—Thank you for giving us the opportunity of replying to Dr Moore's letter concerning the interactions between i.v. atropine and subsequent i.v. injection of a test dose containing adrenaline 15 ug [1]. We totally agree with the fact that the rate of injection through a standard extradural catheter cannot exceed 0.2 ml s"1. Nevertheless, in our daily practice, a test dose may be administered through either the catheter or the Tuohy needle. Thus, in the latter situation, the rate of the injection (1 ml s"1) in our study may correspond to the "reality". Indeed, the "standard test dose" described by Moore and Batra [2] mentioned a rate of injection of 1 ml s"1, corresponding to an injection through the Tuohy needle. The administration of atropine increased the sensitivity of the test dose from 83 % to 91 %, which implies that it does not conceal but improves, even if moderately, the response to adrenaline. Moreover, the majority of vagal attacks occur during the extradural puncture, whereas those which occur following the administration of the therapeutic dose of local anaesthetics remain exceptional (as pointed out by Dr Moore). Thus the sequence that Dr Moore advises seems difficult to accept, as i.v. atropine is used mainly to prevent vagal attacks occurring during extradural puncture. P. NARCHI Paris
REFERENCES 1. Narchi P, Mazoit JX, Cohen S, Samii K. Heart rate response to an i.v. test dose of adrenaline and lignocaine with and without atropine pretreatment. British Journal of Anaesthesia 1991; 66: 583-586. 2. Moore DC, Batra MS. The components of an effective test dose prior to epidural block. Anesthesiology 1981; 55: 693-696.
POTASSIUM IN THE PERIOPERATIVE PERIOD Sir,—Dr Vaughan's review of potassium in the perioperative period [1] advocates immediate hyperventilation in the management of an acute increase in plasma potassium (as identified from the ECG) after suxamcthonium, on the basis that alkalosis encourages potassium ions to enter cells. From investigations using intermittent blood sampling [2], this would appear correct.
Downloaded from http://bja.oxfordjournals.org/ at University of Leeds on May 17, 2015
Sir,—We were interested in the paper by Drs Dunne and Kox, describing symptoms of overdosage in a patient receiving an extradural infusion of bupivacaine [1]. They advised on the recommended dosage for such infusions and suggested measuring plasma concentrations during extended infusions. The authors did not comment on whether or not a loading dose was given to produce an initial measurable block, pain relief or improvement in ventilation. The purpose of a loading dose is to create an initial neuronal block which, being followed by an infusion, maintains the effective concentration of local anaesthetic within the neurone. Attempting to initiate a block using an infusion alone would result in a very slow increase in concentration at neuronal level and hence, an extremely slow onset of block. Theoretically, the rate of removal of local anaesthetic solution from the extradural space is such that a block may never be achieved within non-toxic plasma concentrations using a "buildup" infusion technique of this nature. Had an adequate block been established in the first instance with a suitable loading dose, it would then have been possible to ascertain whether or not subsequent failure of the block was caused by regression of the block or outward migration of the catheter. Tachyphylaxis should have been considered also as a cause of failure in an infusion of long duration, especially where pain has not been adequately captured. Interestingly, they saw no cardiovascular changes. In a volunteer study giving i.v. bupivacaine, Scon and colleagues [2] observed measurable cardiovascular changes in the presence of mild neurological symptoms and low plasma concentrations of bupivacaine. Monitoring the cardiovascular system and the degree of analgesia would be a cheaper and easier alternative to measuring plasma concentrations of bupivacaine.
CORRESPONDENCE
Sir,—I am grateful for the comments of Drs Seex and Eldridge on my review of management of hyponatraemia. In the study reported by Nelson and colleagues [1], 10 of 12 patients with intracranial disease had hyponatraemia associated with plasma volume correction, whilst in the remaining two patients plasma volume was expanded, suggesting ADH-induced water retention. However, even where evidence for volume contraction could be demonstrated, free water clearance was clearly impaired, as the normal physiological response to a reduction in serum sodium would be an increase in free water clearance and correction of dilutional hyponatraemia. The mechanism for reduced free water clearance is probably ADH release in response to extracellular volume contraction, rather than increased extracellular tonicity [2], although local renal mechanisms may also play a role [3]. It seems likely, therefore, that hyponatraemia secondary to cerebral salt wasting reflects an appropriate physiological response to extracellular fluid volume contraction (table I in my review), rather than inappropriate secretion of ADH. Hyponatraemia in this situation, therefore, does not differ from that observed in any condition characterized by sodium depletion. However, the important point raised still stands. Where there is unequivocal evidence of extracellular fluid volume contraction, the correct therapy is repletion rather than water restriction. It should be borne in mind that hyponatraemia in some patients with cerebral disease may also be attributable to inappropriate ADH secretion [1,4]. In this situation water restriction is the first appropriate therapy. It is important to distinguish, therefore, between these two quite different clinical situations, both of which result in hyponatraemia. J. D. SWALES
Leicester REFERENCES 1. Nelson PB, Seif SM, Maroon JC, Robinson AG. Hyponatraemia in intracranial disease: perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Journal of Neurosurgery 1981; 55: 938-941. 2. Leaf A, Mamby AR. Antidiuretic mechanism not regulated by extracellular tonicity. Journal of Clinical Investigation 1952; 31: 60-71. 3. Harrington AR. Hyponatremia due to sodium depletion in the absence of vasopressin. American Journal of Physiology 1972; 222: 768-774. 4. Haden HT, Knox GW. Cerebral hyponatremia with inappropriate antidiuretic hormone syndrome. American Journal of Medical Science 1965; 249: 381-390.
" NEEDLE-THROUGH-NEEDLE " TECHNIQUE FOR COMBINED SPINAL-EXTRADURAL ANAESTHESIA IN OBSTETRICS Sir,—We were interested to read recent correspondence concerning combined spinal-extradural anaesthesia in obstetrics [1,2]. At Queen Charlotte's and Chelsea Hospital, we use the necdle-through-needle technique preferentially and arc currently evaluating various aspects with a prospective trial. We agree with Dr Kestin that placing the patient in a lateral position is to be favoured, to minimize the effects of hypotension, and with Dr Brownridge that the mothers need complete attention after the subarachnoid injection. If the extradural catheter fails to thread after the spinal injection, we abandon insertion attempts and turn the mother as soon as possible onto her other side to produce a bilateral block. We consider a unilateral block to be a failure. We then commence an infusion of ephedrine to avoid hypotension [3] and then we insert an extxadural catheter without hurry. This does not lead to significant delay starting surgery, and avoids the uncertainty of dose requirements in the extradural space having to be superimposed on a poor subarachnoid block. Less clear to us, though, is the difficulty of testing the position of the extradural catheter placed after the spinal has been performed and it is this matter in particular that we feel needs to be addressed. To protect the mother against the problems of accidental i.v. injection, the top-ups we give contain 0.5% bupivacaine with 1 in 200000 adrenaline and 2% lignocaine in equal proportions. Use of lignocaine has been suggested to diminish the cardiotoxicity of bupivacaine [4]. The adrenaline may produce tachycardia if given i.v., although this is questioned [5]. We feel the needle-through-needle technique has an important place in obstetric practice, for both routine and emergency situations [6]. It appears to us that the problems are fairly minor and the advantages of speed, efficacy and flexibility are wholly desirable in an emergency. M. J. G. FAMILTON B. M. MORGAN
London
1. 2. 3. 4. 5. 6.
REFERENCES Brownridge P. Spinal anaesthesia in obstetrics. British Journal of Anaesthesia 1991; 67: 663. Kestin IG. Spinal anaesthesia in obstetrics. British Journal of Anaesthesia 1991; 67: 663. Kang YG, Abouleish E, Caritis S. Prophylactic intravenous ephedrine infusion during spinal anesthesia for Cesarean anesthesia. Anesthesia and Analgesia 1982; 62: 839-842. De Jong RN, Bonin JD. Mixtures of local anesthetics arc no more toxic than parent drugs. Anesthesiology 1989; 54: 177-181. Leighton BL, Norris MC. The test dose revisited again. Anesthesiology 1988; 68: 87. Carrie LES. Extradural, spinal or combined block for obstetric surgical anaesthesia. British Journal of Anaesthesia 1990; 65: 225-223.
"NEUROLOGICAL" COMPLICATIONS OF EXTRADURAL BUPIVACAINE Sir,—Drs Dunne and Kox [1] describe a patient with a combination of respiratory and cerebral signs after a road traffic accident. The cerebral signs are ascribed to a systemic reaction to an extradural infusion of bupivacaine given for pain relief. I would suggest that the most likely cause of the features seen in this patient was a fat embolism syndrome—a diagnosis that must always be kept in mind when a patient develops signs of cerebral irritation after orthopaedic trauma, and a diagnosis made usually by exclusion. I must indicate, therefore, why I would exclude bupivacaine as the primary cause of the problem. First, the clinical features of the reaction were not those associated with systemic toxicity to local anaesthetic drugs, although I accept that the response to chronic administration may not be the same as in the acute, "accidental" situation. Second, the authors refer to the "rapid clearance" of bupivacaine in their patient after the infusion was stopped, yet note that it took more
Downloaded from http://bja.oxfordjournals.org/ at University of Leeds on May 17, 2015
3. Schwartz WB, Bennett W, Curelop S, Bamer FC. A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. American Journal of Medicine 1957; 23: 529-542. 4. Nelson PB, Seif SM, Maroon JC, Robinson AG. Hyponatremia in intracranial disease: perhaps not the syndrome of innappropriate secretion of antidiuretic hormone (SIADH). Journal of Neurosurgery 1981; 55: 938-941. 5. Rosenfeld JV, Barnett GH, Sila CA, Little JR, Bravo EL, Beck GJ. The effect of subarachnoid hemorrhage on blood and CSF atrial natriuretic factor. Journal of Neurontrgery 1989; 71: 32-37. 6. Weinand ME, O'Boynick PL, Goetz KL. A study of serum anridiuretic hormone and atrial natriuretic peptide levels in a series of patients with intracranial disease and hyponatremia. Neurosurgery 1989; 25: 781-785. 7. Fox, JL, Falik JL, Shaloub RJ. Neurosurgical hyponatremia. The role of antidiuresis. Journal of Neurosurgery 1971; 34: 506-514. 8. Lolin Y, Jackowski A, Symon L. Disordered salt and water regulation in neurosurgical practice: modern managment perspectives. Journal of Neurology, Neurosurgery and Psychiatry 1991: (in press). 9. Wijdicks EFM, Vermeulen M, Hijdra A, van Gijn J. Hyponatracmia and cerebral infarction in patients with ruptured intracranial aneurysms. Is fluid restriction harmful? Annals of Neurology 1985; 17: 137-140.
BRITISH JOURNAL OF ANAESTHESIA
328 than 72 h for the clinical condition to resolve. Third, the peak concentration measured (4 mg litre"1) is large, but is noted not infrequently in kinetic studies of regional anaesthesia with bupivacaine, with unremarkable effects. In this regard, the authors may have been led astray by the opinion they received on plasma concentrations from the New Cross Poisons Unit. To indicate that plasma concentrations of bupivacaine should not exceed 1 mg litre"1 is, I am afraid, a pronouncement without foundation. J. A. W. WlLDSMITH Edinburgh
REFERENCE 1. Dunne NM, Kox WJ. Neurological complications following the use of continuous extradural analgesia with bupivacaine. British Journal of Anaesthesia 1991; 66: 617-619.
3 ml and adrenaline 15 ng was not very sensitive for detecting intravascular injection, as moderate or false negative responses occurred frequently" [1]. Should this prohibit them from administering a test dose on the basis that "...atropine 0.5 mg is used routinely in our institution before extradural block is performed, in order to prevent bradycardia"? [1]. Why not: 1) administer the test dose; 2) take the time (2 min) to evaluate it; 3) give 0.5 mg of atropine i.v.; and 4) then immediately follow it with the therapeutic dose of the local anaesthetic ? Doing so would still give i.v. atropine 5 min to suppress "vagal bradycardia". When a therapeutic dose of a local anaesthetic is injected into the lumbar area of the extradural space, it seldom results in a bradycardia until 5 min or more elapses. Therefore, would not administration of atropine in the suggested sequence allow "the best of two worlds", namely, ruling out the possibility of a systemic toxic reaction or a total spinal anaesthetic by the test dose and avoiding a vagal bradycardia by i.v. atropine? D. C. MOORE
G. JONES M. LOGAN Edinburgh
REFERENCES 1. Dunne NM, Kox WJ. Neurological complications following the use of continuous cxtradural analgesia with bupivacaine. British Journal of Anaesthesia 1991; 66: 617-619. 2. Scott DB, Lee A, Fagan D, Bowler GMR, Bloomfield P, Lundh R. Acute toxicity of ropivacaine compared with that of bupivacaine. Anesthesia and Analgesia 1989; 69: 563-569.
ATROPINE AND THE TEST DOSE Sir,—Narchi and colleagues stated: "To be useful, a test dose must be both specific and sensitive. The lack of specificity has already been demonstrated in parturients who exhibited false positive responses to an adrenaline test dose (increases in HR [heart rate] after injection of bupivacaine without adrenaline)" [1]. To support this statement, they cited Cartwright, McCarrol and Antzaka [2]. Evidently they were unaware that the validity of that study was questionable. Its methodology was based on 3 ml of solution being injected through plastic tubing (catheter) at 1 ml s"1, which is impossible [3]. As to sensitivity, Narchi and colleagues found that atropine 0.5 mg i.v. 5 min before "a test dose containing 2% lignocaine
Seattle REFERENCES 1. Narchi P, Mazoit JX, Cohen S, Samii K. Heart rate response to an i.v. test dose of adrenaline and lignocaine with and without atropine pretrcatment. British Journal of Anaesthesia 1991; 66: 583-586. 2. Cartwright PD, McCarrol SM, Antzaka C. Maternal heart rate changes with a plain epidural test dose. Anesthesiology 1986; 65: 226-228. 3. Moore DC, Batra MS, Bridenbaugh LD, Brown DL, Carpenter RL, Hecker BR, Ramsey D. Maternal heart rate changes with a plain epidural test dose—validity of results open to question. Anesthesiology 1987; 66: 854. Sir,—Thank you for giving us the opportunity of replying to Dr Moore's letter concerning the interactions between i.v. atropine and subsequent i.v. injection of a test dose containing adrenaline 15 ug [1]. We totally agree with the fact that the rate of injection through a standard extradural catheter cannot exceed 0.2 ml s"1. Nevertheless, in our daily practice, a test dose may be administered through either the catheter or the Tuohy needle. Thus, in the latter situation, the rate of the injection (1 ml s"1) in our study may correspond to the "reality". Indeed, the "standard test dose" described by Moore and Batra [2] mentioned a rate of injection of 1 ml s"1, corresponding to an injection through the Tuohy needle. The administration of atropine increased the sensitivity of the test dose from 83 % to 91 %, which implies that it does not conceal but improves, even if moderately, the response to adrenaline. Moreover, the majority of vagal attacks occur during the extradural puncture, whereas those which occur following the administration of the therapeutic dose of local anaesthetics remain exceptional (as pointed out by Dr Moore). Thus the sequence that Dr Moore advises seems difficult to accept, as i.v. atropine is used mainly to prevent vagal attacks occurring during extradural puncture. P. NARCHI Paris
REFERENCES 1. Narchi P, Mazoit JX, Cohen S, Samii K. Heart rate response to an i.v. test dose of adrenaline and lignocaine with and without atropine pretreatment. British Journal of Anaesthesia 1991; 66: 583-586. 2. Moore DC, Batra MS. The components of an effective test dose prior to epidural block. Anesthesiology 1981; 55: 693-696.
POTASSIUM IN THE PERIOPERATIVE PERIOD Sir,—Dr Vaughan's review of potassium in the perioperative period [1] advocates immediate hyperventilation in the management of an acute increase in plasma potassium (as identified from the ECG) after suxamcthonium, on the basis that alkalosis encourages potassium ions to enter cells. From investigations using intermittent blood sampling [2], this would appear correct.
Downloaded from http://bja.oxfordjournals.org/ at University of Leeds on May 17, 2015
Sir,—We were interested in the paper by Drs Dunne and Kox, describing symptoms of overdosage in a patient receiving an extradural infusion of bupivacaine [1]. They advised on the recommended dosage for such infusions and suggested measuring plasma concentrations during extended infusions. The authors did not comment on whether or not a loading dose was given to produce an initial measurable block, pain relief or improvement in ventilation. The purpose of a loading dose is to create an initial neuronal block which, being followed by an infusion, maintains the effective concentration of local anaesthetic within the neurone. Attempting to initiate a block using an infusion alone would result in a very slow increase in concentration at neuronal level and hence, an extremely slow onset of block. Theoretically, the rate of removal of local anaesthetic solution from the extradural space is such that a block may never be achieved within non-toxic plasma concentrations using a "buildup" infusion technique of this nature. Had an adequate block been established in the first instance with a suitable loading dose, it would then have been possible to ascertain whether or not subsequent failure of the block was caused by regression of the block or outward migration of the catheter. Tachyphylaxis should have been considered also as a cause of failure in an infusion of long duration, especially where pain has not been adequately captured. Interestingly, they saw no cardiovascular changes. In a volunteer study giving i.v. bupivacaine, Scon and colleagues [2] observed measurable cardiovascular changes in the presence of mild neurological symptoms and low plasma concentrations of bupivacaine. Monitoring the cardiovascular system and the degree of analgesia would be a cheaper and easier alternative to measuring plasma concentrations of bupivacaine.
