I.V. dexamethasone is equivalent to perineural dexamethasone in prolonging the analgesic duration of a single-shot ISB with ropivacaine. As dexamethasone is not licensed for perineural use, clinicians should consider i.v. administration of dexamethasone to achieve an increased duration of ISB.

SummaryWe recruited patients scheduled for shoulder rotator cuff repair or subacromial decompression under general anaesthesia and interscalene brachial plexus blockade (30 ml ropivacaine 0.5%). We allocated 240 participants into four groups of 60 that were given pre-operative saline 0.9% or dexamethasone 1.25 mg, 2.5 mg or 10 mg, intravenously. We recorded outcomes for 48 h. The median (IQR [range]) time to first postoperative analgesic request after saline was 12.2 (11.0-14.1 [1.8-48]) h, which was extended by intravenous dexamethasone 2.5 mg and 10 mg to 17.4 (14.9-21.5 [7.2-48]) h, p < 0.0001, and 20.1 (17.2-24.3 [1.3-48]) h, p < 0.0001, respectively, but not by dexamethasone 1.25 mg, 14.0 (12.1-17.7 [2.1-48]) h, p = 0.05. Postoperative analgesia was given sooner after rotator cuff repair than subacromial decompression, hazard ratio (95% CI) 2.2 (1.6-3.0), p < 0.0001, but later in older participants, hazard ratio (95% CI) 0.98 (0.97-0.99) per year, p < 0

Perineural dexamethasone has a ceiling dose of 4 mg for prolongation of analgesia duration after injection of long-acting local anaesthetic for peripheral nerve block, but evidence for doses < 4 mg is lacking. This randomised controlled triple-blind trial tested the hypothesis that increasing doses of perineural dexamethasone between 1 mg and 4 mg would prolong the duration of analgesia in a dose-dependent manner. Eighty ASA physical status 1-2 patients scheduled for shoulder arthroscopy under general anaesthesia with ultrasound-guided interscalene brachial plexus block were randomly allocated to receive saline (control), dexamethasone 1 mg, 2 mg, 3 mg and 4 mg, together with 20 ml ropivacaine 0.5%. Postoperative analgesia consisted of paracetamol, diclofenac and oxycodone on request, using a pre-defined protocol. The primary outcome was the duration of analgesia, defined as the time between the block procedure and the first analgesic request. Secondary outcomes included rest and dynamic pain scores, and analgesic consumption at 2 h, 24 h and 48 h postoperatively. An analysis of the dose-response relationship was performed using multiple comparison procedure-modelling. The median (IQR [range]) duration of analgesia was significantly prolonged in a dose-dependent manner: control

SummaryA 57-year-old man with recurrent depression, resistant to drug therapy, was scheduled for a course of eight electroconvulsive therapy treatments. The patient had undergone seven treatments without incident over the previous 3 weeks. Immediately following the final treatment, the patient suffered cardiovascular collapse, culminating in cardiac arrest with electromechanical dissociation. Despite resuscitative measures, the patient died. Post-mortem examination found the cause of death to be cardiac tamponade, secondary to cardiac rupture.Keywords Anaesthesia; electroconvulsive therapy. Complication; death. Heart; rupture.. ..................................................................................... Correspondence to: Dr P. B. Ali Accepted: 13 March 1997 Electroconvulsive therapy (ECT) remains widely used in psychiatric practice. Primarily a treatment for endogenous depression resistant to drug therapy, it has been used with variable degrees of success in the treatment of other psychiatric disorders [1, 2]. It has been estimated that over 200 000 ECT treatments are performed each year in the UK [3]. Both the physical and the physiological consequences of the induced seizure are attenuated, to a variable degree, by provision of general anaesthesia and muscular paralysis; this 'modified ECT' is considered to be safe. While associated with minor morbidity, the estimated mortality is low and varies between 0.003 and 0.03% [1, 2]. Cardiovascular complications are the main cause of mortality. Case historyA 57-year-old male with a recurrent depression resistant to drug therapy was scheduled for a course of eight ECT treatments. Co-operative, although vague, the patient reported no serious medical problems and there were no adverse cardiac risk factors. Base line blood analyses were normal and the ECG showed sinus rhythm with normal axis and no evidence of conduction block or ischaemia. His medication at the time of treatment was carbamazepine 200 mg bd. and moclobemide 300 mg bd.Before each treatment the morning dose of moclobemide was omitted.Seven previous treatments had been completed without serious incident. For the final treatment, as before, intravenous access was secured and patient monitoring attached (noninvasive blood pressure, ECG and oximetry). After pre-oxygenation, anaesthesia was induced with etomidate 20 mg and a 40 mg dose of suxamethonium was given. Unilateral ECT was performed and resulted in a modified seizure lasting 27 s. An oropharyngeal airway was then inserted and manual ventilation of the lungs with high flow oxygen was continued.Shortly following treatment, the patient's face was noted to have become congested. This observation coincided with that of an unrecordable blood pressure and an impalpable carotid pulse. The ECG displayed sinus rhythm (rate of 112 beat.min -1) and the pulse oximeter registered 97% saturation. Electromechanical dissociation (EMD) was diagnosed and cardiac massage was immediately started. Despite efforts to resuscitate the patient, his ECG deteriorat...