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 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,
