Although its original clinical description dates from 1873, 1 fat embolism syndrome remains a diagnostic challenge for clinicians. The term fat embolism indicates the often asymptomatic presence of fat globules in the lung parenchyma and peripheral circulation after long bone or other major trauma. The majority (95%) of cases occur after major trauma. Fat embolism syndrome is a serious consequence of fat emboli producing a distinct pattern of clinical symptoms and signs. It is most commonly associated with fractures of long bones and the pelvis, and is more frequent in closed, rather than open, fractures. The incidence increases with the number of fractures involved. Thus, patients with a single long bone fracture have a 1-3% chance of developing the syndrome, but it has been reported in up to 33% of patients with bilateral femoral fractures. 2 Fat embolism syndrome can also occur in relation to other trauma, for example, soft tissue injury, liposuction, bone marrow harvest (Table 1). Non-trauma-related causes (e.g. acute pancreatitis, sickling crisis) are less likely to lead to fat embolism syndrome compared with those associated with trauma. An overall mortality of 5-15% has been described. 3 Clinical presentation Fat embolism syndrome typically presents 24-72 h after the initial injury. Rarely, cases occur as early as 12 h or as much as 2 weeks later. 4 Patients present with a classic triad: (i) respiratory changes; (ii) neurological abnormalities; (iii) petechial rash.

SummaryIn a double-blind, randomised trial, we compared the effects of pretreatment with midazolam at two different doses (0.025 and 0.05 mg.kg 21 ), with placebo, on the induction dose requirements of propofol in two different age groups. We enrolled 120 patients: 60 younger patients (aged 18± 35 years) and 60 older patients (aged over 60 years). All patients received 0.75 m g.kg 21 of fentanyl, plus a blinded pretreatment with either saline or one of two doses of midazolam. Induction continued with a fixed rate infusion of propofol. Propofol dose requirement was recorded, as were cardiovascular parameters and the occurrence of significant apnoea (. 60 s). Midazolam pretreatment was associated with a significant reduction in propofol dose requirement in both younger and older patients. The reduction in older patients was significantly greater than the equivalent response in younger groups. There was no demonstrable benefit in terms of improved cardiovascular stability or reduction in the incidence of apnoea. Caution is advised in the use of midazolam as an agent for co-induction with propofol in the elderly.

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We have used continuous and concurrent monitoring of arterial oxygen saturation (SpO2) and ECG to study the relationship between hypoxaemia and silent myocardial ischaemia in the perioperative period in 11 patients with cardiovascular disease. Ischaemic and hypoxaemic events occurred in all patients. Many events were shortlived and occurred independently of each other. However, our results suggest a close correlation between the duration of hypoxaemia and myocardial ischaemia. Ischaemia is more likely to occur if an episode of hypoxaemia is prolonged (beyond 5 min; P less than 0.01, chi square) and severe (SpO2 less than 85%; P less than 0.05, chi square).

The effect of changing the rate of infusion of propofol for induction of anaesthesia was studied in 60 elderly patients. Propofol was administered at 300, 600 or 1200 ml h-1 until loss of consciousness (as judged by loss of verbal contact with the patient) had been achieved. The duration of induction was significantly longer (P less than 0.001) with the slower infusion rates (104, 68 and 51 s), but the total dose used was significantly less (P less than 0.001) in these patients (1.2, 1.6 and 2.5 mg kg-1, respectively). The decrease in systolic and diastolic arterial pressure was significantly less in the 300-ml h-1 group at the end of induction and immediately after induction (P less than 0.01). The incidence of apnoea was also significantly less in the slower infusion group.

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The time taken for the oxygen saturation (SpO2) to decrease to 90% after preoxygenation was studied in six morbidly obese patients and six matched controls of normal weight. During apnoea the obese patients maintained Spo2 greater than 90% for 196 (SD 80) s (range 55-208 s), compared with 595 (SD 142) s (range 430-825 s) in the control group (P less than 0.001). One patient in the obese group had desaturation before the onset of complete relaxation and tracheal intubation, without complications. Bedside lung function tests were not significantly different between groups and cannot be used as a predictor of the effectiveness of preoxygenation.

Esmolol is a beta 1-selective adrenoceptor blocker that is rapidly metabolized by blood and liver esterases. The beta-receptor and hemodynamic effects of esmolol were determined in a group of 12 healthy men and were compared with those induced by both oral and intravenous propranolol. Esmolol was rapidly effective in inducing at least 90% of steady-state beta-blockade within 5 minutes of either initiating or changing the esmolol infusion rate. More importantly, when esmolol infusion was discontinued the beta-blockade had totally disappeared by 18 minutes after esmolol, 300 micrograms/kg/min, and had been reduced by 50% after 750 micrograms/kg/min. In contrast, 30 minutes after discontinuation of a propranolol infusion, there was no change in the level of beta-blockade. Propranolol was much more potent at blocking isoproterenol-induced tachycardia (dose ratio 33.5 +/- 2.5) than was even the highest dose (750 micrograms/kg/min) of esmolol (dose ratio 13.1 +/- 1.0). The same dose of intravenous propranolol was approximately equipotent to oral propranolol, 40 mg every 8 hours (dose ratio 33.5 +/- 2.5 and 34.5 +/- 3.6, respectively). In contrast, propranolol, 40 mg every 8 hours, and esmolol, 300 micrograms/kg/min, were equipotent in antagonizing exercise-induced tachycardia (40.1% +/- 2.3% and 42.7% +/- 3.2%, respectively). Esmolol had striking hypotensive effects. Systolic blood pressure fell by 20 mm Hg during esmolol infusions of 750 micrograms/kg/min. Esmolol appears to be a potent beta 1-selective adrenoceptor antagonist with a particularly strong hypotensive effect. It is likely to be very useful in the treatment of hemodynamically unstable patients and may be useful in the emergency treatment of hypertension.