1014
Correspondence
gastric stasis had led to fermentation and manual inflation had forced oxygen into the stomach and the explosive mixture had tracked up the oesophagus into the mask. A static spark occurred as the mask was removed from the face thus igniting the mixture. As long ago as 1980 gas analysis from the stomach of a patient with pyloric stenosis had revealed the following: carbon dioxide 56.0%; hydrogen 28.0%; methane 6.8%; air 9.2%; total combustible gases 34.8%. Although Sellick’s manoeuvre has been introduced since the 1954 article appeared, patients may swallow repeatedly during pre-oxygenation and allow mixing of oxygen with fermented gases. We thus have a couple of minutes during which the same conditions occur as they did in 1952 with the exception of antistatic precautions. If we remove this
last factor then what is to stop history repeating itself! How would we stand legally in this event bearing in mind that the danger has been known for so long? D r Gally’s article, despite reporting this tragic event, is full of wit and humour and 1 recommend it to everyone. East Surrey Hospital, Redhill RHI 5 R H
J.E. HAMMOND
Reference [I] GALLYA. Combustible gases generated in the alimentary tract and other hollow viscera and their relationship to explosions occurring during anaesthesia. Erifish Journal of Anaesthesia 1954; 26 189-93.
Hysteria: a cause for opisthotonus Professor Adams’ interesting report of hysteria causing a failure to recover after anaesthesia (Anaesthesia 1991; 4 6 932-4), prompts me to report a similar case of hysterical conversion following an elective repeat oesophageal dilatation. The patient was a 49-year-old nursery nurse with a known history of a pharyngeal web. She had been depressed and was taking amitryptiline 150 mg at night, but was otherwise fit and well. She denied any previous anaesthetic problems. Routine pre-operative investigations were normal. The patient’s old notes were unavailable; nevertheless the surgical team were confident of the diagnosis and so the operation proceeded. Premedication consisted of oral temazepam 20 mg, and anaesthesia was induced with propofol 120 mg, followed by atracurium 25 mg. The trachea was intubated and anaesthesia maintained with isoflurane 1% in nitrous oxide 67% and oxygen 33%. Following the procedure, when the patient was awake and breathing adequately, she was transferred to the recovery ward. Shortly afterwards she appeared to have a generalised tonic-clonic seizure, followed by a 10 min hypertonic stage during which she developed profound opisthotonus. This was relieved by an incremental dose of midazolam 7.5 mg at which point she opened her eyes and responded to simple comments. Her blood sugar and biochemistry were normal. The patient subsequently suffered over 30 similar episodes lasting between 5 and 70 min. During attacks there was no change in the respiratory pattern, Spo, (97-98%) or blood pressure. The majority of attacks resolved spontaneously but prolonged events were treated successfully with bolus doses of midazolam (2.5-7.5 mg). Intravenous procyclidine 10 mg was used on two occasions but produced no discernible effect. Between attacks the patient was sleepy, but a full neurological examination was otherwise normal, with no signs of persisting hypertonicity. She was reviewed by a consultant physician who diagnosed
an acute dystonic reaction, probably drug induced. Centrally acting antidopaminergic drugs are usually implicated in such reactions, but no drug of this type had been administered. Propofol, however, has been reported to cause similar though short lived idiosyncratic reactions [I]. After 24 h the frequency and severity of the opisthotonus was increasing, associated with a rise in CPK to 980 IU, so the patient was transferred to the ITU. Only then were her old case notes finally located. These revealed that in addition to the history volunteered, she had attended the pain clinic on many ocasions because of chronic backache. She had eventually been discharged because of the persistent psychological component to her symptoms. Moreover, her old anaesthetic charts revealed that she had experienced two previous episodes of seizures and opisthotonus lasting a few hours following general anaesthesia. O n one occasion these were witnessed by a consultant neurologist who felt that they were hysterical in nature and would resolve spontaneously. We told the patient that we now had this information, following which she had no further episodes. She subsequently made a complete recovery and will be reviewed by the psychiatrists. This patient showed the typical features of hysterical conversion described by Adams and Goroszeniuk. Unfortunately she also highlights the potential pitfalls of proceeding with surgery when old notes are unavailable. St. Thomas Hospital,
London SEI 7EH
P.A.
STODDART
R.S. GILL M. LIM
Reference [ I ] SAUNDERSPRI, HARRISMNE. Opisthotonus and other neurological sequelea after outpatient anaesthesia. Anaesthesia 1990: 45 552-7.
Hypocapnia and mental function I read with interest the original article by Jhaveri (Anaesthesia 1989; 44: 635-40) which concerned the effects of hypocapnic ventilation on mental function in elderly patients undergoing cataract surgery. The study concluded that these patients, when their lungs were ventilated to a mean Paco, of 2.9 kPa for a mean period of 47.4 min, showed no impairment of psychological function as measured 4 days and 4 weeks after the operation. The study gives no account of whether there was any
such impairment in the recovery ward or on the first postoperative day. It appears that further investigation is required to show that hypocapnic ventilation does not cause postoperative confusion in this important period. Until then, I would question the value of hyperventilating patients to such a low Paco,, requiring fresh gas flows of up to 20 Lmin-’, when it has been shown that normacapnic IPPV anaesthesia lowers intra-ocular pressure and provides satisfactory operating conditions [I-31.
Correspondence
gastric stasis had led to fermentation and manual inflation had forced oxygen into the stomach and the explosive mixture had tracked up the oesophagus into the mask. A static spark occurred as the mask was removed from the face thus igniting the mixture. As long ago as 1980 gas analysis from the stomach of a patient with pyloric stenosis had revealed the following: carbon dioxide 56.0%; hydrogen 28.0%; methane 6.8%; air 9.2%; total combustible gases 34.8%. Although Sellick’s manoeuvre has been introduced since the 1954 article appeared, patients may swallow repeatedly during pre-oxygenation and allow mixing of oxygen with fermented gases. We thus have a couple of minutes during which the same conditions occur as they did in 1952 with the exception of antistatic precautions. If we remove this
last factor then what is to stop history repeating itself! How would we stand legally in this event bearing in mind that the danger has been known for so long? D r Gally’s article, despite reporting this tragic event, is full of wit and humour and 1 recommend it to everyone. East Surrey Hospital, Redhill RHI 5 R H
J.E. HAMMOND
Reference [I] GALLYA. Combustible gases generated in the alimentary tract and other hollow viscera and their relationship to explosions occurring during anaesthesia. Erifish Journal of Anaesthesia 1954; 26 189-93.
Hysteria: a cause for opisthotonus Professor Adams’ interesting report of hysteria causing a failure to recover after anaesthesia (Anaesthesia 1991; 4 6 932-4), prompts me to report a similar case of hysterical conversion following an elective repeat oesophageal dilatation. The patient was a 49-year-old nursery nurse with a known history of a pharyngeal web. She had been depressed and was taking amitryptiline 150 mg at night, but was otherwise fit and well. She denied any previous anaesthetic problems. Routine pre-operative investigations were normal. The patient’s old notes were unavailable; nevertheless the surgical team were confident of the diagnosis and so the operation proceeded. Premedication consisted of oral temazepam 20 mg, and anaesthesia was induced with propofol 120 mg, followed by atracurium 25 mg. The trachea was intubated and anaesthesia maintained with isoflurane 1% in nitrous oxide 67% and oxygen 33%. Following the procedure, when the patient was awake and breathing adequately, she was transferred to the recovery ward. Shortly afterwards she appeared to have a generalised tonic-clonic seizure, followed by a 10 min hypertonic stage during which she developed profound opisthotonus. This was relieved by an incremental dose of midazolam 7.5 mg at which point she opened her eyes and responded to simple comments. Her blood sugar and biochemistry were normal. The patient subsequently suffered over 30 similar episodes lasting between 5 and 70 min. During attacks there was no change in the respiratory pattern, Spo, (97-98%) or blood pressure. The majority of attacks resolved spontaneously but prolonged events were treated successfully with bolus doses of midazolam (2.5-7.5 mg). Intravenous procyclidine 10 mg was used on two occasions but produced no discernible effect. Between attacks the patient was sleepy, but a full neurological examination was otherwise normal, with no signs of persisting hypertonicity. She was reviewed by a consultant physician who diagnosed
an acute dystonic reaction, probably drug induced. Centrally acting antidopaminergic drugs are usually implicated in such reactions, but no drug of this type had been administered. Propofol, however, has been reported to cause similar though short lived idiosyncratic reactions [I]. After 24 h the frequency and severity of the opisthotonus was increasing, associated with a rise in CPK to 980 IU, so the patient was transferred to the ITU. Only then were her old case notes finally located. These revealed that in addition to the history volunteered, she had attended the pain clinic on many ocasions because of chronic backache. She had eventually been discharged because of the persistent psychological component to her symptoms. Moreover, her old anaesthetic charts revealed that she had experienced two previous episodes of seizures and opisthotonus lasting a few hours following general anaesthesia. O n one occasion these were witnessed by a consultant neurologist who felt that they were hysterical in nature and would resolve spontaneously. We told the patient that we now had this information, following which she had no further episodes. She subsequently made a complete recovery and will be reviewed by the psychiatrists. This patient showed the typical features of hysterical conversion described by Adams and Goroszeniuk. Unfortunately she also highlights the potential pitfalls of proceeding with surgery when old notes are unavailable. St. Thomas Hospital,
London SEI 7EH
P.A.
STODDART
R.S. GILL M. LIM
Reference [ I ] SAUNDERSPRI, HARRISMNE. Opisthotonus and other neurological sequelea after outpatient anaesthesia. Anaesthesia 1990: 45 552-7.
Hypocapnia and mental function I read with interest the original article by Jhaveri (Anaesthesia 1989; 44: 635-40) which concerned the effects of hypocapnic ventilation on mental function in elderly patients undergoing cataract surgery. The study concluded that these patients, when their lungs were ventilated to a mean Paco, of 2.9 kPa for a mean period of 47.4 min, showed no impairment of psychological function as measured 4 days and 4 weeks after the operation. The study gives no account of whether there was any
such impairment in the recovery ward or on the first postoperative day. It appears that further investigation is required to show that hypocapnic ventilation does not cause postoperative confusion in this important period. Until then, I would question the value of hyperventilating patients to such a low Paco,, requiring fresh gas flows of up to 20 Lmin-’, when it has been shown that normacapnic IPPV anaesthesia lowers intra-ocular pressure and provides satisfactory operating conditions [I-31.
