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Nitrous Oxide in Sedation and Regional Anaesthesia
- Narendra B Siddaiah (11 March 2008)
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Marked hypotension with low dose remifentanil infusion
- Carl J Morris, Michael B. Dobson (1 February 2008)
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Dexmedetomidine
- Michael G Irwin (10 January 2008)
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Narendra B Siddaiah
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Dear Editor The review article on ‘Sedation and regional anaesthesia in the adult patient’ by D. Hohener is quite informative. However I found it incomplete without mentioning the role of nitrous oxide. Nitrous oxide has been used to provide sedation and analgesia for patients in Accidents and Emergency department, ambulances, dental clinics and for labour analgesia. Oxygen-nitrous oxide sedation has been found to retain the airway reflexes avoiding the risk of aspiration.1. Nitrous oxide produced less behavioral changes, good analgesia quicker recovery and lesser adverse effects.2. Also nitrous oxide has the potential advantages of reducing amounts of intravenous sedative drugs resulting in less likelihood of problems from their side-effects, and fast recovery and discharge time.3. The pollution effects could be minimized by the use of active scavenging, appropriate storage of gas cylinders and training in the technique of administration to remind patients to breathe through the nose and not mouth.4. As adults are normally nose breathers unlike children, the risk is less when compared to children receiving nitrous oxide. Also conscious sedation with sevoflurane in adults using a nasal mask has been found to be within the limits of occupational standards.5. In summary, as there is no single drug that qualifies an ideal sedative agent, it is important to use balanced anaesthetic techniques involving intravenous and/or inhalation agents understanding the needs of the patient and complexities of the disease process resulting in minimal harm to the patient. References: 1. Roberts GJ, Wignall BK. Efficacy Of The Laryngeal Reflex During Oxygen-Nitrous Oxide Sedation (Relative Analgesia). Br J Anaesth 1982; 54: 1277-81 2. Luhmann JD, et al. A Randomized Comparison of Nitrous Oxide Plus Hematoma Block Versus Ketamine Plus Midazolam for Emergency Department Forearm Fracture Reduction in Children. Pediatrics 2006; 118: e1078-86 3. Lahoud GY, Hopkins PM. Balanced conscious sedation with intravenous induction and inhalational maintenance for patients requiring endoscopic and/or surgical procedures. Eur J Anaesthesiol 2007; 24:116-21 4. Holroyd I. Conscious sedation in pediatric dentistry. A short review of the current UK guidelines and the technique of inhalational sedation with nitrous oxide. Paediatr Anaesth 2008; 18: 13–17 5. Hoerauf KH, et al. Occupational exposure to sevoflurane during sedation of adult patient. Int Arch Occup Env Health 1999; 72: 174-7 Conflict of Interest:None declared |
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Carl J Morris, Anaesthetic SpR , Michael B. Dobson
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Editor – We read with interest the review article by D. Höhener and colleagues on sedation and regional anaesthesia in adult patients, and also the randomized controlled trial by M. R. Rai and colleagues comparing remifentanil and propofol target-controlled infusion for conscious sedation in awake fibreoptic intubation. We agree with the statement from the review regarding remifentanil, that “haemodynamic instability is rarely seen at the dosage used for conscious sedation”. In the trial paper there were no adverse events associated with target concentrations of 2.8 – 3.5 ng ml-1. We have experienced however, profound hypotension resulting from very low dose remifentanil infusion. A 49 year old man (weight: 78kg; height: 1.64 m) presented for left carotid endarterectomy following a stroke. His past medical history included hypercholesterolaemia and hypertension. He was otherwise well, with good exercise tolerance, no previous hospital admissions, and was opioid naive. He had never smoked, and consumed about 6 units of alcohol a week. His medications comprised simvastatin, losartan, aspirin, amlodipine and dipyridamole. Initial readings were: heart rate (HR) 93 beats min-1, arterial pressure (ABP) 146/89 mmHg and oxygen saturation of 95% on room air. A 50 mcg ml-1 remifentanil infusion was started at 7 ml hour-1 (75 ng kg-1 min- 1), and oxygen was administered at 4 litres min-1 via Hudson mask, while combined superficial and deep cervical plexus blocks were performed. Shortly after commencing the infusion, the patient reported feeling “distant”. His heart rate slowed to 45 beats min-1 and his ABP dropped to 60/30 mmHg. He remained in communication. Respiratory rate (monitored via ECG electrode impedance), and oxygen saturations were unchanged. Assuming that this was a vagal response to the injections we waited briefly, and then administered 600 mcg intravenous atropine. His heart rate rose gradually to 60 beats min-1, but his arterial pressure continued to fall to 50/31 mmHg (non invasive 70/40 mmHg). He became diaphoretic, but remained in communication and reported feeling “drifty”. We informed him of his low ABP, placed him head down, administered a fluid bolus, and stopped the remifentanil infusion. Over the next 5 minutes, the patient’s HR increased to 95 beats min-1, his ABP to 118/68 mmHg and he felt back to normal. We felt that his hypotension and bradycardia were most likely a transient complication of the block. Therefore we restarted the remifentanil infusion at 5mls hour-1 (53 ng kg-1 minute-1) and prepared to go into theatre. However, despite maintaining a heart rate over 85 beats min-1, his ABP again began to fall. On this occasion reaching 66/44 mmHg. Again the patient remained comfortable and calm. We stopped the remifentanil infusion, administered 0.5 mg intravenous metaraminol and called in the surgeon. The patient’s ABP gradually returned to its previous level. There was a discussion between patient, anaesthetists and surgeon about the implication of these two episodes. We were concerned that the patient may have been particularly sensitive to movements or pressure on the neck, and therefore may not be able to tolerate the surgical procedure. As his haemodynamic parameters remained normal, despite further movements of the head and neck, it was decided to proceed without sedation. The patient remained comfortable throughout his operation, with no further analgaesia required. Surgery was straight forward. In order to assess whether remifentanil may have been implicated in his hypotensive episodes, the infusion was restarted cautiously in theatre at 1ml hour-1 (11 ng kg-1 min-1). This was prior to cross clamping, during uneventful surgery and ABP had remained stable for over 30 minutes. Within 3 minutes of starting the infusion, ABP had fallen from 125/76 mmHg to 87/53 mmHg. The infusion was stopped at this point, and after transiently falling to 72/44 mmHg, ABP rose steadily back to 124/74 mmHg over the next 8 minutes. This patient had three hypotensive episodes, with a strong temporal association to the administration of a remifentanil infusion. Using the pharmacokinetic model in the Alaris PK pump, estimated end target concentrations of remifentanil would have been 2 ng ml-1, 1.6 ng ml-1, and 0.4 ng ml-1 respectively at the three different infusion rates used during the procedure. Other potential causes for our patient’s hypotension were considered and rejected (carotid sinus effects, drug error, pump error). The most likely explanation, is that this patient was particularly sensitive to the hypotensive effects of remifentanil. As well as a type A drug reaction, there will of course have been some contribution from his antihypertensive mediations. We do not know if propofol sedation would have caused a similar response. Nor do we know if this reaction was general to opioids as we advised their avoidance in the post operative period. Since its introduction remifentanil has gone on to establish its role in a variety of clinical situations. It has proved particularly useful in the context of awake carotid artery surgery. Side effects have generally been predictable, and often related more to respiratory depression, with remifentanil offering good haemodynamic stability. Our patient tolerated marked hypotension with no long term sequelae. We would be interested to know if anyone else has had similar experiences. Despite a wide variation in dose responses, we have not seen such an exaggerated haemodynamic change on initiation of remifentanil infusion before. We were surprised that the profound cardiovascular depression did not seem to be associated with significant respiratory depression, judged by oximetry and respiratory rate monitoring. There is current interest in the use of remifentanil sedation regimes in intensive care settings. Clearly this is a group of patients where a similar response could have far more serious consequences. C. J. Morris M. B. Dobson Oxford Email: carljmorris@googlemail.com Conflict of Interest:None declared |
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Michael G Irwin, Head Dept of Anaesthesiology, University of Hong Kong
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I read with interest the review of sedation and regional anaesthesia in the adult patient by Höhener and colleagues. I felt, however, that little attention was given to the increasing importance of the alpha-2 agonist dexmedetomidine in this setting. Dexmedetomidine has high alpha-2 selectivity compared to clonidine and has been the subject of numerous clinical studies in the past decade. I strongly disagree with the comment that it has not "found its way into routine use for sedation in regional anaesthesia". I understand that this may apply to Europe where the drug is not available but, since BJA is an international journal, it certainly doesn't apply to the rest of the world where, in many places, it has become the drug of first choice in this setting. Dexmedetomidine was originally developed as a sedative and analgesic agent for use in intensive care. However, it has a number of unique pharmacodynamic properties which also make it useful perioperatively. Unlike gabaminergic drugs, sedation is mediated via the locus coeruleus. This induces electroencephalographic activity similar to natural sleep thereby allowing facilitated arousal and avoiding patient disorientation and facilitating cooperation. Thus it is particularly useful in operations such as endovascular procedures, awake craniotomy and carotid endarterectomy under regional anaesthesia. The drug also reduces catecholamine secretion, decreasing stress, inducing neuroprotection and leading to a modest (10- 20%) reduction in heart rate and blood pressure, which may be particularly beneficial in patients with cardiovascular disease (certainly not "significant haemodynamic impairment"). Alpha-2 receptors in the dorsal horn induce analgesia without respiratory depression and we have personally not, with extensive use, seen any patient develop nausea and vomiting (there is good scientific evidence to the contrary). This drug has an important role in the practice of sedation and anaesthesia. We have also found that the drug can be reliably administered intranasally and, as such, is useful in premedication. 1.Irwin MG, Wong GTC. Dexmedetomidine: handbook of clinical applications.2006 Lippincott Williams & Wilkins ISBN 0781771358. 2. McCutcheon CA, Orme RM, Scott DA, Davies MJ, McGlade DP. A comparison of dexmedetomidine versus conventional therapy for sedation and hemodynamic control during carotid endarterectomy performed under regional anesthesia. Anesth Analg 2006; 102:668-75. 3. Bekker AY, Basile J, Gold M, Riles T, Adelman M, Cuff G, Mathew JP, Goldberg JD. Dexmedetomidine for awake carotid endarterectomy: efficacy, hemodynamic profile, and side effects. J Neurosurg Anesthesiol. 2004 Apr;16(2):126-35. 4. Khasawinah TA, Ramirez A, Berkenbosch JW, Tobias JD. Preliminary experience with dexmedetomidine in the treatment of cyclic vomiting syndrome. Am J Ther 2003; 10: 303-7. 5. Mack PF, Perrine K, Kobylarz E, Schwartz TH, Lien CA. Dexmedetomidine and neurocognitive testing in awake craniotomy. J Neurosurg Anesthesiol 2004; 16: 20-5. 6. A double blind crossover assessment of the sedative and analgesic effects of intranasal dexmedetomidine. Yuen VM, Irwin MG, Hui TW, Yuen MK, Lee HY. Anesth Analg 2007; 105: 374-80. 7. A comparison of dexmedetomidine and midazolam for sedation during wisdom teeth extraction. Cheung CW, Ying CLA, Chiu WK, Wong GTC, Ng JKF, Irwin MG. Anaesthesia 2007;62: 1132-8. 8. Yuen VM, Hui TW, Irwin MG, Yuen MK. A comparison of intranasal dexmedetomidine and oral midazolam for premedication in pediatric anesthesia – A double-blind randomized controlled trial. Anesth Analg, in press. Conflict of Interest:None declared |
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