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bation facilitated by vecuronium 0.2 mg·kg–1 iv. Anesthesia was maintained using sevoflurane 1.0 to 3.0% and N2O 66% in oxygen. At the end of surgery, patients received intravenously, in a randomized, double-blinded manner, placebo (Intralipid®) or propofol at three different doses (0.25, 0.5 and 0.75 mg·kg–1); (n = 20 each). Residual neuromuscular blockade was antagonized with atropine 0.02 mg·kg–1 iv and neostigmine 0.04 mg·kg–1 iv, and the trachea was extubated. Postoperatively, all episodes of nausea, retching and vomiting from 0 to 24 hr after anesthesia were recorded.3 Statistical analyses were performed using ANOVA, Chi-square test, and Fisher’s exact probability test. A P < 0.05 was considered significant. Values are presented as mean ± SD or number (%). The treatment groups were comparable with respect to demographic data. The rate of emetic symptoms from 0 to 24 hr after anesthesia was less in patients who had received propofol 0.5 mg·kg–1 (15%) or 0.75 mg·kg–1 (15%) than in those who had received placebo (60%); (P < 0.05). However, there was no difference between propofol 0.25 mg·kg–1 (55%) and placebo (Table available as Additional Material at www.cja-jca.org). To our knowledge, this is the first report to determine the minimum effective dose of propofol for the prevention of PONV following thyroidectomy. Propofol 0.5 mg·kg–1 administered intravenously at the end of surgery is the minimum effective dose for prophylaxis against PONV. The precise mechanism by which propofol acts as an antiemetic remains unclear, but there is a possibility that propofol may have a weak serotonin antagonistic effect.4 Propofol at small doses, less than 1.0 mg·kg–1, lacks sedative, dysphoric, and extrapyramidal signs.5 Mitsuko Numazaki MD Yoshitaka Fujii MD University of Tsukuba Institute of Clinical Medicine, Tsukuba, Japan E-mail:
[email protected] References 1 Dejonckheere M, Deloof T, Dustin N, Ewalenko P. Alizapride in the prevention of post-thyroidectomy emetic sequelae. Eur J Anaesthesiol 1990; 7: 421–7. 2 Borgeat A, Winder-Smith OH, Saiah M, Rifat K. Subhypnotic doses of propofol possess direct antiemetic properties. Anesth Analg 1992; 74: 539–41. 3 Fujii Y, Tanaka H, Kobayashi N. Small doses of propofol, droperidol, and metoclopramide for the prevention of postoperative nausea and vomiting after thyroidectomy. Otolaryngol Head Neck Surg 2001; 124: 266–9. 4 Hammas B, Hvarfner A, Thorn SE, Wattwil M. Effects
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of propofol on ipecacuanha-induced nausea and vomiting. Acta Anaesthesiol Scand 1998; 42: 447–51. 5 Smith I, White PF, Nathanson M, Gouldson R. Propofol. An update on its clinical use. Anesthesiology 1994; 81: 1005–43.
Severe hypotension following spinal anesthesia in a patient treated with risperidone To the Editor: We describe a case of profound hypotension during spinal anesthesia in a patient treated with risperidone that was partially refractory to conventional treatment with large doses of ephedrine and iv fluids. A 69-yr-old woman was scheduled for repair of hip fracture. She was 161 cm, weighed 72 kg and had no allergies. Her medical history included diabetes mellitus and vascular dementia. Medications included insulin and risperidone 2 mg. The patient was given 1 mg etomidate and was placed in the sitting position. Spinal anesthesia was achieved successfully on the first attempt at L3–L4, using a 25-gauge spinal needle. Thirteen milligrams of 0.5% hyperbaric bupivacaine were administered leading to a T9 block. Ten minutes later, there was a profound decrease in blood pressure from baseline 142/90 to 72/43 mmHg. Oxygen saturation remained at 98%. Initial interventions included 1000 mL of Ringer’s lactate solution and 50 mg of ephedrine iv in of 5 mg increments over the ensuing 20 min. There was only a minor improvement of blood pressure to 82/51 mmHg, without a heart rate increase. Other interventions included 500 mL of 6% hetastarch and 50 mg of ephedrine iv in of 10 mg increments over the ensuing 20 min and vital signs gradually improved to baseline. The patient had no overt symptoms such as lightheadedness or nausea during the episode. Risperidone is an atypical antipsychotic medication with both 5-HT2 receptor and D2 dopamine receptor antagonism, but also possesses affinity for both α1 and α2-adrenoceptors and can cause hypotension. It is used for the treatment of behavioural and psychological symptoms in patients with dementia because it reduces delusions, aggression and agitation without severe extrapyramidal symptoms. Orthostatic hypotension and tachycardia due to anticholinergic or α1-adrenoreceptor blockade may occur in the majority of patients at therapeutic dosages of antipsychotic drugs.1 Depletion of presynaptic norepinephrine stores and α-adrenergic antagonism by antipsychotic
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medication should be considered when profound hypotension occurs during spinal anesthesia. Only one prior case has been published describing profound hypotension in a parturient with bipolar disease, controlled with lithium and risperidone, undergoing spinal anesthesia for Cesarean delivery. The patient was refractory to conventional treatment with ephedrine and iv fluids, and eventually responded to large doses of phenylephrine.2 The treatment should consist of iv fluids and sympathomimetic drugs. Epinephrine and dopamine are not recommended, as ß-stimulation may worsen hypotension due to risperidone-induced α-adrenergic antagonism. Antoni Arxer Tarrés MD Antonio Villalonga MD PhD Hospital Universitari Doctor Josep Trueta, Catalonia, Spain E-mail:
[email protected] References 1 Buckley NA, Sanders P. Cardiovascular adverse effects of antipsychotic drugs. Drug Saf 2000; 23: 215–28. 2 Williams JH, Hepner DL. Risperidone and exaggerated hypotension during a spinal anesthetic. Anesth Analg 2004; 98: 240–1.
Intraoperative neuromonitoring in cardiac surgical patients with severe cerebrovascular disease To the Editor: Patients with severe cerebrovascular disease are at a high risk of neurologic complications during cardiac surgery, as a result of cerebral embolization or hypoperfusion during cardiopulmonary bypass (CPB). Intraoperative neuromonitoring, including transcranial Doppler ultrasound (TCD) and electroencephalography (EEG), may be particularly useful in patients with cerebrovascular disease.1 We hereby present two cases that illustrate the use of intraoperative neuromonitoring during cardiac surgery in patients with severe cerebrovascular disease. Patient A suffered a recent right cerebellar stroke and had high-grade obstructing lesions in the right subclavian, right vertebral and mid-basilar arteries, and no posterior communicating arteries. Patient B had a complete occlusion of the right internal carotid artery (ICA) and a 90% stenosis of the left ICA. Both patients were referred for coronary artery bypass graft surgery (CABG) with severe triple vessel coronary disease. Due to the risk of inadequate cerebral perfusion
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FIGURE A discharge of high-intensity transient signals (HITS) and brief rise in cerebral blood flow at aortic unclamping (upper figure). This was associated with a transient period of electroencephalography (EEG) slowing (lower figure).
during CPB, intraoperative neuromonitoring techniques were employed for each patient. After anesthetic induction, electrodes were positioned to continuously record EEG activity. Doppler probes were placed on each temporal window to monitor blood flow in the middle cerebral arteries (MCA). A tight control of cerebral perfusion was ensured with mean systemic blood pressures above 80 mmHg and CPB flows above 5.5 L·min–1. Doppler monitoring of Patient A revealed symmetric flow in both middle cerebral arteries that increased during CPB. A discharge of 53 high-intensity transient signals (HITS) was detected when the aorta was unclamped, followed by a transient period of EEG slowing, but without localized changes on the EEG (Figure). Patient B’s Doppler examination revealed flow in both MCA and flow in the opposite direction at the level of the posterior communicating artery, suggesting collateral flow to the anterior circulation from the vertebrobasilar system. No changes indicative of hypoperfusion were identified during Patient B’s surgery. Following CABG, each patient had an uneventful postoperative course free of neurologic injury. Recognition of cerebral hypoperfusion or emboli using neuromonitoring techniques represents an important advance in the prevention of neurologic complications during cardiac surgery. Through the appearance of excessive slow-wave activity, intraoperative EEG can detect a disturbance of cerebrocortical function suggestive of inadequate cerebral perfusion or oxygenation. However, additional monitoring is required to identify the etiology of EEG slowing since cerebrocortical depression resulting from ischemia
