1098
Correspondence Transient ischaemic attack following carbon dioxide retention due to intrathecal morphine
A 76-year-old man with a history of chronic obstructive airways disease, angina and three previous transient ischaemic attack (TIAs) developed respiratory depression after pleurectomy. Pre-operative blood gases breathing air were as follows: pH 7.34,Pao, 10 kPa, Paco, 4.3 kPa. He received an anaesthetic consisting of propofol, atracurium and nitrous oxide in oxygen supplemented by isoflurane. Analgesia was provided by intrathecal morphine 2 mg injected at the level of L,, after induction. Peri-operative management was uneventful and the patient went to the recovery ward following tracheal extubation. He was pain free, fully awake and had a respiratory rate of 18 min-' with an oxygen saturation of 99% breathing 40% oxygen. He was returned to the thoracic ward as all high dependency and intensive care beds had been taken up by emergencies. Written instructions to monitor respiratory rate and level of sedation half hourly were issued. He was transferred to the high dependency unit 3 h later when a bed became available. He was found to be heaviliy sedated, responding only to pain and the right arm was paralysed. Respiratory rate was 20 min-I, and breathing was shallow and uncoordinated. Oxygen saturation was 95% breathing 40% oxygen. He had pinpoint pupils, a good pulse volume and a blood pressure of 120/75mmHg. A 12-lead ECG showed sinus rhythm with multiple ventricular ectopics. He responded to 400 pg naloxone intravenously with an increased respiratory effort and dilated pupils. Neurological examination confirmed loss of power in the right arm with loss of reflexes. Blood gases showed a respiratory acidosis (Paco, 8.6 kPa and Pao, 16.4 kPa). His conscious level again deteriorated but responded to further naloxone. He was transferred to the intensive care unit where he stayed overnight breathing spontaneously, treated with naloxone and doxapram infusions. Overnight the Paco, progressively decreased from 8.8 to 4.5 kPa. As his respiratory function improved
so did the function of his right arm, which by the following morning was completely normal. This patient developed respiratory failure following what was in retrospect a rather large dose of spinal morphine [I]. Of particular interest is the nature of the transient ischaemic attack (TIA). The patient had a compromised cerebral circulation. Further enquiry showed that his previous TIAs gave rise to similar episodes of right monoparesis indicating a localised area of cerebral hypoperfusion. A possible explanation for the TIA is that cerebral vasodilation due to hypercapnia may have induced a condition of vascular steal as described by Brawley [2]. However, one recent study [3] found no evidence of steal during hypothermic cardiopulmonary bypass in patients with cerebrovascular disease. Other more mundane explanations, such as transient hypotension or cerebral emboli, may explain the neurological signs. The correlation of improvement in the neurological state and reduction in Pacoz suggests intracerebral steal as the underlying pathophysiology . C. IP YAM J. SALT
Charing Cross Hospital,
London W6 8 R F References
[I] ETCHES RC, SANDLER AN, DALEY MD. Respiratory depression and spinal opioids. Canadian Journal of Anae.ythesiu 1989; 3 6 165-85. [2] BRAWLEYBW. The pathophysiology of intracerebral steal following carbon dioxide inhalation, an experimental study. Scandinuvian Journal of Laboraiory and Clinical Investigation 1968; Suppl. 102. [3] GRAVLEE GP, ROY RC, STUMP DA, HUDSPETHAS, ROGERS AT, PROUGHDS. Regional cerebrovascular reactivity to carbon dioxide during cardiopulmonary bypass in patients with cerebrovascular disease. Journal of Thoracic and Cardiovascular Surgery 1990; 99: 1022-9.
Low-flow anaesthesia systems, charcoal and isoflurane kinetics Since washout kinetics of inhalational anaesthetics are longer with low-flow anaesthesia systems, it is generally accepted that they are better suited for prolonged surgery where the 'margin of safety', in terms of time, is longer than short procedures. A proposed 'rule of thumb' is that for every hour of anaesthesia, anaesthetic vapours should be stopped 15 min before the anticipated end of surgery [I] (i.e. 45 rnin for a 3 h operation). However, this is too risky to apply in practice because of the risk of too early awakening. Fortunately, washout kinetics can be greatly accelerated by inclusion of a charcoal filter into the breathing system. Twenty subjects (age: 51.6, S D 14.5years), scheduled for extra and intracranial surgery (duration: 171.2, S D 63.5 min; minimum: 90 min-maximum: 340 min) were studied. All patients were premedicated with diazepam 0.15 mg.kg- I orally or hydroxizine 50 mg intramuscularly. After 5 min pre-oxygenation, anaesthesia was induced with fentanyl 3 pg.kg-l, propofol 1.5 mg.kg-' and atropine 0.01 mg.kg-l. Tracheal intubation was facilitated by vecuronium 120 pg.kg-l. Mechanical ventilation was regulated to maintain an end-tidal CO, 4.0-4.5 kPa with a respiratory rate of 8-12 breaths.min-l, a tidal volume of 10 ml.kg-l and I:E ratio 2 1.2. A mean total fresh gas flow (oxygen and nitrous oxide) of approximately 0.7 1.min-I was used during surgery, with an end-tidal isoflurane concentration of 0.8-1.2Oh.
8 0.6al
e :: - 0.4.t
0.2, 0
I
I
60
I
l
l
I20 I80 Time (s)
240
300
Fig. 1. End-tidal concentration of isoflurane (mean, SD), during the first 5 min after the introduction of charcoal cartridge into the low-flow circuit. The experimental washout curve is accurately described by a logarithmic curve: y = 1.25-0.4 log,, ( x ).
At the end of surgery, all anaesthetic gases were stopped and the inspiratory flow was bypassed through a small cartridge, prefilled with 40 g of charcoal (BDH Ltd, Poole,
Correspondence UK), using the plastic sheet of a filter, Sterivent (DAR, Mirandola-Modena, Italy). Inspiratory and expiratory (end-tidal) isoflurane concentration was measured every 10 s with an Ohmeda RGM 4250 monitor, precalibrated with a gas mixture of known concentration (Anesthesia Calibration Gas, Scott Medical Products, Plumsteadville, PA, USA). The inspiratory concentration of isoflurane declined to very low values (0.065 SD 0.049%) during the first 60 s, decreasing to zero in the following min; end-tidal concentration of isoflurane declined to MAC,,,,, values, according to Gaumann et al. [2], within 5 min of the introduction of the charcoal cartridge. The tracheas of all patients were extubated within this short time interval. The experimental washout curve of end-tidal isoflurane concentration can be accurately described by a logarithmic curve of the form: y = a-log( x ) (Fig. I ) . We used each charcoal cartridge for a maximum of four patients: in a separate, preliminary study, it was Our impression that more prolonged use is accompanied by a progressive, rapid decline of the efficacy of charcoal. The
1099
use of small-volume charcoal cartridges during low-flow anaesthesia, as suggested in this study, make low flow systems more flexible in their use: anaesthetic gas can be stopped at the very end of surgery, and the patients are completely awake in a few minutes. The anaesthesia level is also more easily controllable and accidental overdosing can be immediately controlled. Instituto Polidisciplinare di A nestesia , Universita degii Studi di Trieste, Trieste, Italy
E. ROMANO M. PEGORARO A. VACRI C. PECCHIARI E. Auci
References [ I ] ERNST EA, PEARSON DJ. Principles and practice of closed circuit anesthesia. Advances in Anesthesiology 1987; 4 89-122. DM, MUSTAKIJ-P, TAWNYIE. MAC-awake of [2] GAUMANN isoflurane, enflurane and halothane evaluated bv slow and fast alveolar washout. British Journal ofAnaesthesia*l992;68:81-4.
Bacteraemia following nasopharyngeal airway insertion Nasopharyngeal airways are frequently employed in medical practice. While it has long been established [ I , 21 that nasotracheal intubation causes a transient bacteraemia, thus warranting appropriate antibiotic chemoprophylaxis in patients with cardiac lesions, no such data exist about the use of nasopharyngeal airways. We therefore read with interest the recent article by Ali et al. which reported that the use of oral and nasopharyngeal airways is not associated with bacteraemia (Anaesthesia 1992; 47: 153-5) and would like to report the results of a study which confirms their findings. Thirty-five patients (ASA 1 ) who were undergoing minor surgical procedures under general anaesthesia using a mask were studied. They were assigned to have either a nasopharyngeal airway (study group) or an oropharyngeal airway (control group) inserted. Swabs from the anterior nares were taken from all patients. Ten ml of blood were sampled from an antecubital vein following skin preparation with 70% isopropyl alcohol 30 s and 3 min following insertion of the airway. Five ml were inoculated into both an aerobic and an anaerobic blood culture bottle (‘Bactec system’). The bottles were screened twice daily for 48 h and thereafter once daily for 5 days. Isolates from nasal swabs grew predominantly normal flora, i.e.; Staph. epiderrnidis. Staph. aureus and Strep. viridans. No organisms were isolated from any of the blood cultures. The aetiology of bacteraemia after nasotracheal intubation is thought to be related either to entry of nasopharyngeal commensals into the bloodstream via the
nasal muscosa during passage of the tube or to transfer of nasopharyngeal commensals from a contaminated tracheal tube into the bloodstream via the tracheal mucosa. The finding that insertion of a nasopharyngeal airway does not result in bacteraemia weakens the former theory; rather it lends weight to the theory that it is the presence of a contaminated tube in the trachea allowing passage of organisms through the tracheal mucosa which is responsible for bacteria entering the bloodstream. In conclusion, we found that nasopharyngeal airway insertion, in contrast to nasotracheal intubation, is not associated with a bacteraemia. This coincides with the findings of Ali et al; however, unlike these authors, we see no reason to recommend antibiotic prophylaxis for nasopharyngeal airway insertion in high risk patients. St. Vincent’s Hospital, Elm Park, Dublin 4 , Ireland
R. ROONEY E.J. CRUMMY A.J. MCSHANE
References [ I ] BERRYFA JR, YARBOROUGH N, RUSSELL CM, CARPENTER MA. HENDLEY JO. Transient bacteremia during dental manipulation in children. Pediatrics 1973; 52: 479. [2] MCSHANE AJ. HONE R. Prevention of bacterial endocarditis: does nasal intubation warrant prophylaxis? British Medical Journal 1986; 292 26-7.
Anaesthesia for motor cortical mapping The requirements of anaesthesia for intracranial surgery include a perfcctly still patient who does not cough or strain on the tracheal tube, and a ‘slack’ brain. In addition the patient should wake up quickly after surgery so that a neurological assessment can be performed. These aims are usually achieved by using a techniquc of neuromuscular paralysis with light general anaesthesia. However, for motor cortical mapping, muscle paralysis cannot be used. Techniques that have been employed include awake craniotomy with sedation and local anaesthesia, or general anaesthesia without muscle paralysis. The latter requires
fairly deep anaesthesia to ensure no movement or coughing when the dura is open and the concentration of volatile agent required may produce a swollen brain unless hypocapnoea is induced by hyperventilation [I]. Recovery from anaesthesia will also be delayed. In order to achieve the desired conditions for surgery we used a technique of general anaesthesia with artificial ventilation of the lungs. For the initial part of the proceedure a conventional relaxant technique was used, but during the period of cortical mapping, we used an alfentanil infusion to suppress breathing and coughing.
Correspondence Transient ischaemic attack following carbon dioxide retention due to intrathecal morphine
A 76-year-old man with a history of chronic obstructive airways disease, angina and three previous transient ischaemic attack (TIAs) developed respiratory depression after pleurectomy. Pre-operative blood gases breathing air were as follows: pH 7.34,Pao, 10 kPa, Paco, 4.3 kPa. He received an anaesthetic consisting of propofol, atracurium and nitrous oxide in oxygen supplemented by isoflurane. Analgesia was provided by intrathecal morphine 2 mg injected at the level of L,, after induction. Peri-operative management was uneventful and the patient went to the recovery ward following tracheal extubation. He was pain free, fully awake and had a respiratory rate of 18 min-' with an oxygen saturation of 99% breathing 40% oxygen. He was returned to the thoracic ward as all high dependency and intensive care beds had been taken up by emergencies. Written instructions to monitor respiratory rate and level of sedation half hourly were issued. He was transferred to the high dependency unit 3 h later when a bed became available. He was found to be heaviliy sedated, responding only to pain and the right arm was paralysed. Respiratory rate was 20 min-I, and breathing was shallow and uncoordinated. Oxygen saturation was 95% breathing 40% oxygen. He had pinpoint pupils, a good pulse volume and a blood pressure of 120/75mmHg. A 12-lead ECG showed sinus rhythm with multiple ventricular ectopics. He responded to 400 pg naloxone intravenously with an increased respiratory effort and dilated pupils. Neurological examination confirmed loss of power in the right arm with loss of reflexes. Blood gases showed a respiratory acidosis (Paco, 8.6 kPa and Pao, 16.4 kPa). His conscious level again deteriorated but responded to further naloxone. He was transferred to the intensive care unit where he stayed overnight breathing spontaneously, treated with naloxone and doxapram infusions. Overnight the Paco, progressively decreased from 8.8 to 4.5 kPa. As his respiratory function improved
so did the function of his right arm, which by the following morning was completely normal. This patient developed respiratory failure following what was in retrospect a rather large dose of spinal morphine [I]. Of particular interest is the nature of the transient ischaemic attack (TIA). The patient had a compromised cerebral circulation. Further enquiry showed that his previous TIAs gave rise to similar episodes of right monoparesis indicating a localised area of cerebral hypoperfusion. A possible explanation for the TIA is that cerebral vasodilation due to hypercapnia may have induced a condition of vascular steal as described by Brawley [2]. However, one recent study [3] found no evidence of steal during hypothermic cardiopulmonary bypass in patients with cerebrovascular disease. Other more mundane explanations, such as transient hypotension or cerebral emboli, may explain the neurological signs. The correlation of improvement in the neurological state and reduction in Pacoz suggests intracerebral steal as the underlying pathophysiology . C. IP YAM J. SALT
Charing Cross Hospital,
London W6 8 R F References
[I] ETCHES RC, SANDLER AN, DALEY MD. Respiratory depression and spinal opioids. Canadian Journal of Anae.ythesiu 1989; 3 6 165-85. [2] BRAWLEYBW. The pathophysiology of intracerebral steal following carbon dioxide inhalation, an experimental study. Scandinuvian Journal of Laboraiory and Clinical Investigation 1968; Suppl. 102. [3] GRAVLEE GP, ROY RC, STUMP DA, HUDSPETHAS, ROGERS AT, PROUGHDS. Regional cerebrovascular reactivity to carbon dioxide during cardiopulmonary bypass in patients with cerebrovascular disease. Journal of Thoracic and Cardiovascular Surgery 1990; 99: 1022-9.
Low-flow anaesthesia systems, charcoal and isoflurane kinetics Since washout kinetics of inhalational anaesthetics are longer with low-flow anaesthesia systems, it is generally accepted that they are better suited for prolonged surgery where the 'margin of safety', in terms of time, is longer than short procedures. A proposed 'rule of thumb' is that for every hour of anaesthesia, anaesthetic vapours should be stopped 15 min before the anticipated end of surgery [I] (i.e. 45 rnin for a 3 h operation). However, this is too risky to apply in practice because of the risk of too early awakening. Fortunately, washout kinetics can be greatly accelerated by inclusion of a charcoal filter into the breathing system. Twenty subjects (age: 51.6, S D 14.5years), scheduled for extra and intracranial surgery (duration: 171.2, S D 63.5 min; minimum: 90 min-maximum: 340 min) were studied. All patients were premedicated with diazepam 0.15 mg.kg- I orally or hydroxizine 50 mg intramuscularly. After 5 min pre-oxygenation, anaesthesia was induced with fentanyl 3 pg.kg-l, propofol 1.5 mg.kg-' and atropine 0.01 mg.kg-l. Tracheal intubation was facilitated by vecuronium 120 pg.kg-l. Mechanical ventilation was regulated to maintain an end-tidal CO, 4.0-4.5 kPa with a respiratory rate of 8-12 breaths.min-l, a tidal volume of 10 ml.kg-l and I:E ratio 2 1.2. A mean total fresh gas flow (oxygen and nitrous oxide) of approximately 0.7 1.min-I was used during surgery, with an end-tidal isoflurane concentration of 0.8-1.2Oh.
8 0.6al
e :: - 0.4.t
0.2, 0
I
I
60
I
l
l
I20 I80 Time (s)
240
300
Fig. 1. End-tidal concentration of isoflurane (mean, SD), during the first 5 min after the introduction of charcoal cartridge into the low-flow circuit. The experimental washout curve is accurately described by a logarithmic curve: y = 1.25-0.4 log,, ( x ).
At the end of surgery, all anaesthetic gases were stopped and the inspiratory flow was bypassed through a small cartridge, prefilled with 40 g of charcoal (BDH Ltd, Poole,
Correspondence UK), using the plastic sheet of a filter, Sterivent (DAR, Mirandola-Modena, Italy). Inspiratory and expiratory (end-tidal) isoflurane concentration was measured every 10 s with an Ohmeda RGM 4250 monitor, precalibrated with a gas mixture of known concentration (Anesthesia Calibration Gas, Scott Medical Products, Plumsteadville, PA, USA). The inspiratory concentration of isoflurane declined to very low values (0.065 SD 0.049%) during the first 60 s, decreasing to zero in the following min; end-tidal concentration of isoflurane declined to MAC,,,,, values, according to Gaumann et al. [2], within 5 min of the introduction of the charcoal cartridge. The tracheas of all patients were extubated within this short time interval. The experimental washout curve of end-tidal isoflurane concentration can be accurately described by a logarithmic curve of the form: y = a-log( x ) (Fig. I ) . We used each charcoal cartridge for a maximum of four patients: in a separate, preliminary study, it was Our impression that more prolonged use is accompanied by a progressive, rapid decline of the efficacy of charcoal. The
1099
use of small-volume charcoal cartridges during low-flow anaesthesia, as suggested in this study, make low flow systems more flexible in their use: anaesthetic gas can be stopped at the very end of surgery, and the patients are completely awake in a few minutes. The anaesthesia level is also more easily controllable and accidental overdosing can be immediately controlled. Instituto Polidisciplinare di A nestesia , Universita degii Studi di Trieste, Trieste, Italy
E. ROMANO M. PEGORARO A. VACRI C. PECCHIARI E. Auci
References [ I ] ERNST EA, PEARSON DJ. Principles and practice of closed circuit anesthesia. Advances in Anesthesiology 1987; 4 89-122. DM, MUSTAKIJ-P, TAWNYIE. MAC-awake of [2] GAUMANN isoflurane, enflurane and halothane evaluated bv slow and fast alveolar washout. British Journal ofAnaesthesia*l992;68:81-4.
Bacteraemia following nasopharyngeal airway insertion Nasopharyngeal airways are frequently employed in medical practice. While it has long been established [ I , 21 that nasotracheal intubation causes a transient bacteraemia, thus warranting appropriate antibiotic chemoprophylaxis in patients with cardiac lesions, no such data exist about the use of nasopharyngeal airways. We therefore read with interest the recent article by Ali et al. which reported that the use of oral and nasopharyngeal airways is not associated with bacteraemia (Anaesthesia 1992; 47: 153-5) and would like to report the results of a study which confirms their findings. Thirty-five patients (ASA 1 ) who were undergoing minor surgical procedures under general anaesthesia using a mask were studied. They were assigned to have either a nasopharyngeal airway (study group) or an oropharyngeal airway (control group) inserted. Swabs from the anterior nares were taken from all patients. Ten ml of blood were sampled from an antecubital vein following skin preparation with 70% isopropyl alcohol 30 s and 3 min following insertion of the airway. Five ml were inoculated into both an aerobic and an anaerobic blood culture bottle (‘Bactec system’). The bottles were screened twice daily for 48 h and thereafter once daily for 5 days. Isolates from nasal swabs grew predominantly normal flora, i.e.; Staph. epiderrnidis. Staph. aureus and Strep. viridans. No organisms were isolated from any of the blood cultures. The aetiology of bacteraemia after nasotracheal intubation is thought to be related either to entry of nasopharyngeal commensals into the bloodstream via the
nasal muscosa during passage of the tube or to transfer of nasopharyngeal commensals from a contaminated tracheal tube into the bloodstream via the tracheal mucosa. The finding that insertion of a nasopharyngeal airway does not result in bacteraemia weakens the former theory; rather it lends weight to the theory that it is the presence of a contaminated tube in the trachea allowing passage of organisms through the tracheal mucosa which is responsible for bacteria entering the bloodstream. In conclusion, we found that nasopharyngeal airway insertion, in contrast to nasotracheal intubation, is not associated with a bacteraemia. This coincides with the findings of Ali et al; however, unlike these authors, we see no reason to recommend antibiotic prophylaxis for nasopharyngeal airway insertion in high risk patients. St. Vincent’s Hospital, Elm Park, Dublin 4 , Ireland
R. ROONEY E.J. CRUMMY A.J. MCSHANE
References [ I ] BERRYFA JR, YARBOROUGH N, RUSSELL CM, CARPENTER MA. HENDLEY JO. Transient bacteremia during dental manipulation in children. Pediatrics 1973; 52: 479. [2] MCSHANE AJ. HONE R. Prevention of bacterial endocarditis: does nasal intubation warrant prophylaxis? British Medical Journal 1986; 292 26-7.
Anaesthesia for motor cortical mapping The requirements of anaesthesia for intracranial surgery include a perfcctly still patient who does not cough or strain on the tracheal tube, and a ‘slack’ brain. In addition the patient should wake up quickly after surgery so that a neurological assessment can be performed. These aims are usually achieved by using a techniquc of neuromuscular paralysis with light general anaesthesia. However, for motor cortical mapping, muscle paralysis cannot be used. Techniques that have been employed include awake craniotomy with sedation and local anaesthesia, or general anaesthesia without muscle paralysis. The latter requires
fairly deep anaesthesia to ensure no movement or coughing when the dura is open and the concentration of volatile agent required may produce a swollen brain unless hypocapnoea is induced by hyperventilation [I]. Recovery from anaesthesia will also be delayed. In order to achieve the desired conditions for surgery we used a technique of general anaesthesia with artificial ventilation of the lungs. For the initial part of the proceedure a conventional relaxant technique was used, but during the period of cortical mapping, we used an alfentanil infusion to suppress breathing and coughing.
