- Email: [email protected]
MANAGEMENT OF HYPONATRAEMIA
BRITISH JOURNAL OF ANAESTHESIA
326 that this apparent paradox had to be addressed. We stated that both Libet and Cotterill had proposed that conscious awareness is not necessary for the execution of a simple reaction task. In contrast, we proposed that, in this specific situation (which lies between a conditioned reflex and a voluntary movement), a motor programme might be set up by biasing a set of synapses so that the stimulus automatically triggers the required response. We state that "consciousness is undoubtedly necessary for this programme to be set up and kept in a state of readiness". The later work of Keller and Heckhausen to which Dr Munglani refers is concerned with the initiation of voluntary movements. Whilst this is fascinating in its own right, it is some way from the point of our editorial, which was concerned with conscious awareness. We are sure that Dr Munglani will agree that Libet's work is not familiar to most anaesthetists; nevertheless its wider dissemination will help us to make progress in the difficult problem of understanding and detecting conscious awareness under anaesthesia. J. JESSOP
Cambridge
D. W. RYAN D. BELL
Newcastle upon Tyne EUROPEAN STANDARDISATION COMMITTEE ON ANAESTHETIC EQUIPMENT Sir,—As members of the United Kingdom delegation to the European Standardisation Committee on Anaesthetic Equipment CEN/TC215 and its Working Groups, we would like to point out that reference to a private draft committee document made by Dr Zbinden and his colleagues in their article on fresh gas utilization of eight circle systems [1] has not been authorized by the Technical Committee. The test procedure included in the CEN Committee's working document was that proposed by Dr Zbinden's group. It is possible that the proposed fresh gas utilization test will be deleted or changed substantially before publication of the Standard. Some members of the CEN Working Group have expressed doubts about the value of this test in clinical anaesthesia because, as the authors state, the results can be modified greatly by changes in ventilation volume, flow pattern, compliance of the breathing system, leakage, etc. The design and arrangement of components of a circle system to achieve 100% fresh gas utilization would not improve patient safety if the exhaust valve was badly sited, the system resistance high or the leakage excessive. We therefore request that the reference to CEN/TC215/WG1 N36 is not interpreted as providing published international support for this method of apparatus evaluation. R. GREENBAUM
Member of CEN/TC215 B. R. SUGG
Member of CEN/TC215 B. HAYES
Chairman of CEN/TC21S REFERENCE 1. Zbinden AM, Fcigcnwinter, P, Hutmacher M. Fresh gas utilization of eight circle systems. British Journal of Anaesthesia 1991; 67: 492^199.
INCORRECT STATEMENT Sir,—In my article entitled " Indications for Use of Bicarbonate in Patients with Metabolic Acidosis" [1], I stated that THAM is an experimental drug. It is, in fact, approved for use in humans and has been for several years. A. I. ARIEFF
San Francisco REFERENCE 1. Arieff AI. Indications for use of bicarbonate in patients with metabolic acidosis. British Journal of Anaesthesia 1992; 67: 165-177.
REFERENCE 1. Turner DABT. Blood conservation. British Journal of Anaesthesia 1991; 66: 281-284.
MANAGEMENT OF HYPONATRAEMIA Sir,—We read with interest Professor Swales' review on the management of hyponatraemia [1]. However, we should like to draw attention to a situation he has not discussed, namely hyponatraemia caused by natriuresis initiated by intracranial disease. Although relatively rare, this condition is important, as its management differs from that of other causes of hyponatraemia. The term "cerebral salt wasting" was used first in the early 1950s to explain hyponatraemia in patients after subarachnoid haemorrhage (SAH). The cause was thought to be renal sodium loss [2]. However, after the description of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in 1957, it was assumed widely that water retention was the cause of the (dilutional) hyponatraemia and the term fell into disuse [3]. It was reintroduced in 1981 by Nelson and colleagues, who investigated 12 patients with intracranial pathology who fulfilled established laboratory criteria of SIADH [4]. In 10 of these patients there was a decrease in red cell mass, plasma volume and total blood volume—results which could not be explained by SIADH, as water excess should lead to an expanded circulation in this condition. Natriuresis is a better explanation and cerebral salt wasting a preferable term, as the aetiology is unknown. Cerebral salt wasting has since been reported in many other intracranial pathologies, including disease of the pituitary and its surrounds, head injury and infections including meningitis. Further studies have given support to this concept and atrial natriuretic peptide has been implicated as a possible cause [5-7]. This condition is of more than academic interest, as the treatment of cerebral salt wasting (replace salt and restore circulating volume) is the opposite of fluid restriction used to manage SIADH. Hyponatraemia is common after subarachnoid haemorrhage and recent work indicates that 67 % of these cases are a result of natriuresis and not SIADH [8]. Fluid restriction in any intracranial pathology is potentially dangerous and in SAH increased mortality and morbidity are well documented [9]. Clinicians involved in treating such patients therefore should be aware of this distinction, as inappropriate fluid restriction is hazardous. K. A. SEEX P. R. ELDRIDGE
Liverpool REFERENCES 1. Swales JD. Management of hyponatraemia. British Journal of Anaesthesia 1991; 67: 146-153. 2. Cort JH. Cerebral salt wasting. Lancet 1954; 1: 752-754.
Downloaded from http://bja.oxfordjournals.org/ at University of Winnipeg on September 11, 2015
Doncaster J. G. JONES
BLOOD CONSERVATION Sir,—Dr Turner's editorial on blood conservation [1] dealt with the role of autotransfusion and we wish to comment further. Our experience with the Haemocell 350 system now exceeds 40 patients who have received more than 60 units of salvaged blood. Haemolysis always occurs, but the degree depends on how carefully the surgeon collects salvaged blood, and there is a fast learning curve; it is not clinically significant and does not affect a patient with reasonable renal function. These systems are designed to save red blood cells that would otherwise be discarded, so any cells saved are a bonus. The majority of cells have a perfectly normal survival time. There has been no case of postoperative coagulopathy. Our research indicates that red blood cells passed through a cell washer improve their 2,3-DPG concentrations. Air embolism, loss of platelets and fibrinogen, and microemboli are similar risks to any i.v. transfusions of stored blood. We have been using the system routinely for elective aortic aneurysm, where it makes a beneficial impact on transfusion requirements and gives confidence in using the system in emergency situations.
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 Winnipeg on September 11, 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.
326 that this apparent paradox had to be addressed. We stated that both Libet and Cotterill had proposed that conscious awareness is not necessary for the execution of a simple reaction task. In contrast, we proposed that, in this specific situation (which lies between a conditioned reflex and a voluntary movement), a motor programme might be set up by biasing a set of synapses so that the stimulus automatically triggers the required response. We state that "consciousness is undoubtedly necessary for this programme to be set up and kept in a state of readiness". The later work of Keller and Heckhausen to which Dr Munglani refers is concerned with the initiation of voluntary movements. Whilst this is fascinating in its own right, it is some way from the point of our editorial, which was concerned with conscious awareness. We are sure that Dr Munglani will agree that Libet's work is not familiar to most anaesthetists; nevertheless its wider dissemination will help us to make progress in the difficult problem of understanding and detecting conscious awareness under anaesthesia. J. JESSOP
Cambridge
D. W. RYAN D. BELL
Newcastle upon Tyne EUROPEAN STANDARDISATION COMMITTEE ON ANAESTHETIC EQUIPMENT Sir,—As members of the United Kingdom delegation to the European Standardisation Committee on Anaesthetic Equipment CEN/TC215 and its Working Groups, we would like to point out that reference to a private draft committee document made by Dr Zbinden and his colleagues in their article on fresh gas utilization of eight circle systems [1] has not been authorized by the Technical Committee. The test procedure included in the CEN Committee's working document was that proposed by Dr Zbinden's group. It is possible that the proposed fresh gas utilization test will be deleted or changed substantially before publication of the Standard. Some members of the CEN Working Group have expressed doubts about the value of this test in clinical anaesthesia because, as the authors state, the results can be modified greatly by changes in ventilation volume, flow pattern, compliance of the breathing system, leakage, etc. The design and arrangement of components of a circle system to achieve 100% fresh gas utilization would not improve patient safety if the exhaust valve was badly sited, the system resistance high or the leakage excessive. We therefore request that the reference to CEN/TC215/WG1 N36 is not interpreted as providing published international support for this method of apparatus evaluation. R. GREENBAUM
Member of CEN/TC215 B. R. SUGG
Member of CEN/TC215 B. HAYES
Chairman of CEN/TC21S REFERENCE 1. Zbinden AM, Fcigcnwinter, P, Hutmacher M. Fresh gas utilization of eight circle systems. British Journal of Anaesthesia 1991; 67: 492^199.
INCORRECT STATEMENT Sir,—In my article entitled " Indications for Use of Bicarbonate in Patients with Metabolic Acidosis" [1], I stated that THAM is an experimental drug. It is, in fact, approved for use in humans and has been for several years. A. I. ARIEFF
San Francisco REFERENCE 1. Arieff AI. Indications for use of bicarbonate in patients with metabolic acidosis. British Journal of Anaesthesia 1992; 67: 165-177.
REFERENCE 1. Turner DABT. Blood conservation. British Journal of Anaesthesia 1991; 66: 281-284.
MANAGEMENT OF HYPONATRAEMIA Sir,—We read with interest Professor Swales' review on the management of hyponatraemia [1]. However, we should like to draw attention to a situation he has not discussed, namely hyponatraemia caused by natriuresis initiated by intracranial disease. Although relatively rare, this condition is important, as its management differs from that of other causes of hyponatraemia. The term "cerebral salt wasting" was used first in the early 1950s to explain hyponatraemia in patients after subarachnoid haemorrhage (SAH). The cause was thought to be renal sodium loss [2]. However, after the description of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in 1957, it was assumed widely that water retention was the cause of the (dilutional) hyponatraemia and the term fell into disuse [3]. It was reintroduced in 1981 by Nelson and colleagues, who investigated 12 patients with intracranial pathology who fulfilled established laboratory criteria of SIADH [4]. In 10 of these patients there was a decrease in red cell mass, plasma volume and total blood volume—results which could not be explained by SIADH, as water excess should lead to an expanded circulation in this condition. Natriuresis is a better explanation and cerebral salt wasting a preferable term, as the aetiology is unknown. Cerebral salt wasting has since been reported in many other intracranial pathologies, including disease of the pituitary and its surrounds, head injury and infections including meningitis. Further studies have given support to this concept and atrial natriuretic peptide has been implicated as a possible cause [5-7]. This condition is of more than academic interest, as the treatment of cerebral salt wasting (replace salt and restore circulating volume) is the opposite of fluid restriction used to manage SIADH. Hyponatraemia is common after subarachnoid haemorrhage and recent work indicates that 67 % of these cases are a result of natriuresis and not SIADH [8]. Fluid restriction in any intracranial pathology is potentially dangerous and in SAH increased mortality and morbidity are well documented [9]. Clinicians involved in treating such patients therefore should be aware of this distinction, as inappropriate fluid restriction is hazardous. K. A. SEEX P. R. ELDRIDGE
Liverpool REFERENCES 1. Swales JD. Management of hyponatraemia. British Journal of Anaesthesia 1991; 67: 146-153. 2. Cort JH. Cerebral salt wasting. Lancet 1954; 1: 752-754.
Downloaded from http://bja.oxfordjournals.org/ at University of Winnipeg on September 11, 2015
Doncaster J. G. JONES
BLOOD CONSERVATION Sir,—Dr Turner's editorial on blood conservation [1] dealt with the role of autotransfusion and we wish to comment further. Our experience with the Haemocell 350 system now exceeds 40 patients who have received more than 60 units of salvaged blood. Haemolysis always occurs, but the degree depends on how carefully the surgeon collects salvaged blood, and there is a fast learning curve; it is not clinically significant and does not affect a patient with reasonable renal function. These systems are designed to save red blood cells that would otherwise be discarded, so any cells saved are a bonus. The majority of cells have a perfectly normal survival time. There has been no case of postoperative coagulopathy. Our research indicates that red blood cells passed through a cell washer improve their 2,3-DPG concentrations. Air embolism, loss of platelets and fibrinogen, and microemboli are similar risks to any i.v. transfusions of stored blood. We have been using the system routinely for elective aortic aneurysm, where it makes a beneficial impact on transfusion requirements and gives confidence in using the system in emergency situations.
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 Winnipeg on September 11, 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.