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.
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).
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