718
Correspondence
nurses to follow, with instructions for use of the infusion devices, an observation chart, and a contingency plan for any complications. These methods are employed for all surgical specialties, including thoracic, orthopaedic, general, gynaecological, and urological surgery. We have so far accumulated 287 patients. We have encountered a number of problems. The commonest is discontinuation of the infusion by surgeons, predominantly juniors, because of systemic hypotension. Rather than increase intravenous fluids, the epidural infusion is seen as the cause of the hypotension. We now educate the junior surgeons in the management of epidural infusions. Epidural catheters are often difficult to place accurately, and we have found that up to 10% of our infusions fail because of catheter leaks or migration. Although no patient has experienced severe pain, there have been 19 in whom the epidural has failed to produce adequate analgesia. These are usually transferred to a patient-controlled analgesia system. Any hospital wishing to start epidural infusions should have a reserve of PCA
machines to use in the event of either catheter problems or inadequate analgesia. We have had no instances of respiratory depression, and only three patients where the infusion had to be stopped because of nausea and vomiting. A number of criteria are considered essential for satisfactory management: nurse education and training, which must be repeated frequently because of the high turnover of nursing staff; a designated nurse supervisor on each ward to bring any problems to the fore; a pain relief nurse dedicated each day to acute pain management; a well designed protocol to enable complete observations and awareness of rapidly developing complications; a standardised dosage regimen so that new anaesthetists may feel comfortable in starting this form of analgesia in the out-of-hours period.
Norfolk and Norwich Hospital, Norwich. Norfolk
A. MORIARTY B. JOHNSTON G.E. PORTER
Respiratory depression after alfentanil We present a patient who developed respiratory depression in the recovery room after intra-operative continuous infusion of alfentanil. This complication has already been described following fentanyl, pethidine morphine and sufentanil. A 44-year-old, 72 kg man presented for partial gastrectomy. He had had no other previous illness and preoperative evaluation was unremarkable. An hour before surgery he was premedicated with pethidine 75 mg and promethazine (50mg). Monitoring included ECG, arterial blood pressure pulse oximeter and nerve stimulator. Anesthesia was induced with thiopentone ( 5 mg.kg-I), alfentanil (60 pg.kg-') and atracurium (0.5 mg.kg-I) intravenously. Maintenance was with 66% nitrous oxide, atracurium IOpm.kg-'.min-', and alfentanil 1.5 pg.kg-'.min-' (total dose = 16 mg). The procedure lasted 150 min; atracurium and alfentanil infusions were discontinued 30 min before the end of surgery. The patient was completely awake 5 min after nitrous oxide was stopped, with the train-of-four showing complete recovery and a stable respiratory rate of 12 breath.min-'. His trachea was extubated and no anticholinesterase was given. In the recovery room, he received supplementary oxygen by a nasal cannula (3 I.min-'). Twenty minutes after surgery (50 min after stopping the alfentanil infusion) the patient became apnoeic, unresponsive, rigid and cyanotic with constricted pupils. Naloxane 200 pg resulted in restoration of respiration and recovery of consciousness. He remained in the recovery room for 8 h without any other incident. All opioids produce respiratory depression, but it is rare to see apnoea after a patient is completely awake. Recurrence or delayed respiratory depression has been explained in different ways. The end of surgical stimulus and drowsiness could increase opioid depressor effects. Respiratory acidosis can occur after tracheal extubation, increasing cerebral blood flow and alfentanil nonionized
fraction. All these factors can produce more opioid receptor stimulation [I]. Alfentanil, with a pKa 6.5, will be less influenced by pH than other opioids. Respiratory depression has also been attributed to a second peak in plasma opioid level, as a result of redistribution from peripheral compartments, or rapid intestinal absorption of accumulated opioid [2]. Skeletal muscular mobility and return to normal temperature can also produce redistribution. Mahla et al. described two cases of respiratory depression after alfentanil infusion with similar doses to ours (50 pg.kg-' plus 1.5 pg.kg-'.min-') and at about the same time (45 min after the infusion) [3]. This second peak can also occur during surgery or some hours later [4]. It is important to remember that alfentanil can produce delayed respiratory depression, similar to other opioids, in a dose-dependent manner. The use of this drug, which is especially indicated in outpatient anesthesia because of its short half-life, does not preclude monitoring in a recovery room.
Hospital Puerta de Hierro, San Martin de Porres, 4 , 28035 Madrid. Spain
F. CASSINELLO A. PERAL A. ANDUEZA I. MOURELLE
References [ I ] LULLMANN H, MARTINS BS, PETERST. pH-dependent accumulation of fentanyl, lofentanyl and alfentanil by beating guinea pig atria. Erifish Journal of Anaesfhesia 1985; 57: 1012. [2] STOECKEL H, SCHUTTLER J. MAGNUSSEN H, HENGSTMANN JH.
Plasma fentanyl concentrations and occurrence of respiratory depression in volunteers. British Journal of' Anaesthesia 1982; 54: 1087.
[3] MAHLAME, MAJ MC, WHITESE el a / . Delayed respiratory depression after alfentanil. Anesthesiology 1988; 6 9 593-5. [4] SINGLETON MA, ROSENJI, FISHERDM. Pharmacokinetics of fentanyl for infants and adults. Anesrhesiology 1984; 61: A440.
Evaluation of the E25 for the Level 1 blood warmer I have recently assessed an additional disposable warmer for the Level 1 series, a system for warming large, rapid fluid transfusions [I]. The new warmer (E25) differs from those previously available in that it is not a complete unit, but connects to a
conventional giving set and does not have an air eliminator; it has a conventional flow chamber. These differences mean that the warmer must be primed before insertion into the Level 1 warming unit. This is easily done and it must be ensured that the rigid heat exchanger, as
Correspondence
nurses to follow, with instructions for use of the infusion devices, an observation chart, and a contingency plan for any complications. These methods are employed for all surgical specialties, including thoracic, orthopaedic, general, gynaecological, and urological surgery. We have so far accumulated 287 patients. We have encountered a number of problems. The commonest is discontinuation of the infusion by surgeons, predominantly juniors, because of systemic hypotension. Rather than increase intravenous fluids, the epidural infusion is seen as the cause of the hypotension. We now educate the junior surgeons in the management of epidural infusions. Epidural catheters are often difficult to place accurately, and we have found that up to 10% of our infusions fail because of catheter leaks or migration. Although no patient has experienced severe pain, there have been 19 in whom the epidural has failed to produce adequate analgesia. These are usually transferred to a patient-controlled analgesia system. Any hospital wishing to start epidural infusions should have a reserve of PCA
machines to use in the event of either catheter problems or inadequate analgesia. We have had no instances of respiratory depression, and only three patients where the infusion had to be stopped because of nausea and vomiting. A number of criteria are considered essential for satisfactory management: nurse education and training, which must be repeated frequently because of the high turnover of nursing staff; a designated nurse supervisor on each ward to bring any problems to the fore; a pain relief nurse dedicated each day to acute pain management; a well designed protocol to enable complete observations and awareness of rapidly developing complications; a standardised dosage regimen so that new anaesthetists may feel comfortable in starting this form of analgesia in the out-of-hours period.
Norfolk and Norwich Hospital, Norwich. Norfolk
A. MORIARTY B. JOHNSTON G.E. PORTER
Respiratory depression after alfentanil We present a patient who developed respiratory depression in the recovery room after intra-operative continuous infusion of alfentanil. This complication has already been described following fentanyl, pethidine morphine and sufentanil. A 44-year-old, 72 kg man presented for partial gastrectomy. He had had no other previous illness and preoperative evaluation was unremarkable. An hour before surgery he was premedicated with pethidine 75 mg and promethazine (50mg). Monitoring included ECG, arterial blood pressure pulse oximeter and nerve stimulator. Anesthesia was induced with thiopentone ( 5 mg.kg-I), alfentanil (60 pg.kg-') and atracurium (0.5 mg.kg-I) intravenously. Maintenance was with 66% nitrous oxide, atracurium IOpm.kg-'.min-', and alfentanil 1.5 pg.kg-'.min-' (total dose = 16 mg). The procedure lasted 150 min; atracurium and alfentanil infusions were discontinued 30 min before the end of surgery. The patient was completely awake 5 min after nitrous oxide was stopped, with the train-of-four showing complete recovery and a stable respiratory rate of 12 breath.min-'. His trachea was extubated and no anticholinesterase was given. In the recovery room, he received supplementary oxygen by a nasal cannula (3 I.min-'). Twenty minutes after surgery (50 min after stopping the alfentanil infusion) the patient became apnoeic, unresponsive, rigid and cyanotic with constricted pupils. Naloxane 200 pg resulted in restoration of respiration and recovery of consciousness. He remained in the recovery room for 8 h without any other incident. All opioids produce respiratory depression, but it is rare to see apnoea after a patient is completely awake. Recurrence or delayed respiratory depression has been explained in different ways. The end of surgical stimulus and drowsiness could increase opioid depressor effects. Respiratory acidosis can occur after tracheal extubation, increasing cerebral blood flow and alfentanil nonionized
fraction. All these factors can produce more opioid receptor stimulation [I]. Alfentanil, with a pKa 6.5, will be less influenced by pH than other opioids. Respiratory depression has also been attributed to a second peak in plasma opioid level, as a result of redistribution from peripheral compartments, or rapid intestinal absorption of accumulated opioid [2]. Skeletal muscular mobility and return to normal temperature can also produce redistribution. Mahla et al. described two cases of respiratory depression after alfentanil infusion with similar doses to ours (50 pg.kg-' plus 1.5 pg.kg-'.min-') and at about the same time (45 min after the infusion) [3]. This second peak can also occur during surgery or some hours later [4]. It is important to remember that alfentanil can produce delayed respiratory depression, similar to other opioids, in a dose-dependent manner. The use of this drug, which is especially indicated in outpatient anesthesia because of its short half-life, does not preclude monitoring in a recovery room.
Hospital Puerta de Hierro, San Martin de Porres, 4 , 28035 Madrid. Spain
F. CASSINELLO A. PERAL A. ANDUEZA I. MOURELLE
References [ I ] LULLMANN H, MARTINS BS, PETERST. pH-dependent accumulation of fentanyl, lofentanyl and alfentanil by beating guinea pig atria. Erifish Journal of Anaesfhesia 1985; 57: 1012. [2] STOECKEL H, SCHUTTLER J. MAGNUSSEN H, HENGSTMANN JH.
Plasma fentanyl concentrations and occurrence of respiratory depression in volunteers. British Journal of' Anaesthesia 1982; 54: 1087.
[3] MAHLAME, MAJ MC, WHITESE el a / . Delayed respiratory depression after alfentanil. Anesthesiology 1988; 6 9 593-5. [4] SINGLETON MA, ROSENJI, FISHERDM. Pharmacokinetics of fentanyl for infants and adults. Anesrhesiology 1984; 61: A440.
Evaluation of the E25 for the Level 1 blood warmer I have recently assessed an additional disposable warmer for the Level 1 series, a system for warming large, rapid fluid transfusions [I]. The new warmer (E25) differs from those previously available in that it is not a complete unit, but connects to a
conventional giving set and does not have an air eliminator; it has a conventional flow chamber. These differences mean that the warmer must be primed before insertion into the Level 1 warming unit. This is easily done and it must be ensured that the rigid heat exchanger, as
