We examined the degree of neuroprotection conferred by various concentrations of edaravone on cortical cultures exposed to prolonged hypoxia (24 h) under three conditions: mild hypothermia (32°C), normothermia (37°C), and mild hyperthermia (39°C). The survival of cortical neurones from E16 Wistar rats (SR) was evaluated using photomicrographs taken before and after exposure to hypoxia.

The mean survival of neurones exposed to hypoxia at normothermia was 14.7 (sem 1.8)%. The addition of 50 µM edaravone significantly improved the mean survival to 40.5 (4.7)%. This improvement was noted at higher doses of edaravone (5 µM ≤) but not at lower doses (≤500 nM). With mild hypothermia and prolonged hypoxia without edaravone, neuroprotection was significantly improved with a mean survival of 63.0 (5.2)%. This neuroprotective effect was not enhanced with the addition of edaravone, even at the highest dose. Hypoxia-induced neurotoxicity was aggravated by mild hyperthermia as reflected by a mean survival of 9.1 (2.1)%. However, higher concentrations of edaravone inhibited the deleterious effect of mild hyperthermia, thereby demonstrating a significant neuroprotective effect. The survival of neurones subjected to both hyperthermia and edaravone was the same as that of neurones exposed to normothermia and edaravone.

Temperature is a potential factor in determining whether edaravone confers a neuroprotective effect when applied during prolonged hypoxic insults.

The study pertains to a randomized double-blind study with blinded adjudication of outcomes. Patients requiring surgery for an isolated hip fracture of less than 48 h received saline or tranexamic acid 15 mg kg^–1 given at skin incision and 3 h later. Primary efficacy outcome was erythrocyte transfusion from surgery up to day 8. Transfusion was administered according to a standardized protocol (Hb<9 g dl^–1). Safety criterion was a composite of symptomatic and asymptomatic vascular events up to 6 weeks.

Fifty-seven patients were randomized to tranexamic acid and 53 to placebo. The rate of erythrocyte transfusion was 42% with tranexamic acid and 60% with placebo (P=0.06). Preoperative haemoglobin value, age, and type of surgery were risk factors for erythrocyte transfusion independent of treatment group. The probability of vascular events at 6 weeks was 16% in the tranexamic acid group and 6% in the placebo group (P=0.10). A meta-analysis combining this study with previous trials showed that tranexamic acid significantly reduced erythrocyte transfusion in hip fracture surgery although efficacy was lower than that observed in hip or knee arthroplasty.

In hip fracture surgery, tranexamic acid reduces erythrocyte transfusion but may promote a hypercoagulable state. Thus, further evaluation of safety is required before recommending the off-label use of tranexamic acid.

Eighty-eight patients, mean (sd) age 39.3 (7.7) yr, who underwent thoracotomy between the age of 0 and 25 yr were asked to recall the duration of postoperative pain and—if pain was still present—to describe intensity and character of pain. In addition, all patients underwent quantitative sensory testing.

Fourteen patients (16%) recalled that their postoperative pain had lasted for more than 3 months: one (3.2%) patient in the youngest group (0–6 yr), seven (19.4%) patients in the age group 7–12 yr, and six (28.5%) patients in the age group 13–25 yr (P=0.03). Three out of the 14 patients, who were 11, 11, and 18 yr of age at the time of surgery, still had pain at present. Quantitative sensory testing revealed hypo- and hyperphenomena in most patients, including those with persistent pain. Tactile detection thresholds and pressure detection thresholds were significantly lower on the operated side when compared with the contralateral side (n=88; P<0.001).

The risk of developing chronic pain after thoracotomy seems to be lower if surgery is performed at a young age. Pain after thoracotomy is likely to be of neuropathic origin.

Forty-five piglets were randomized into three groups. After induction of general anaesthesia using sevoflurane and peripheral venous cannulation, the trachea was intubated, the lungs were artificially ventilated, and anaesthesia was maintained by sevoflurane. Under steady state 0.2 ml kg^–1 and after 10 min 0.4 ml kg^–1 of one of the following three test solutions was administered i.v.: bupivacaine 0.125% (Group 1), bupivacaine 0.125%+epinephrine 1:200 000 (Group 2), and plain epinephrine 1:200 000 (Group 3). The ECG was analysed for alterations in heart rate and T-elevation.

After injection of 0.2 or 0.4 ml kg^–1 test solution, an increase in heart rate of at least 10% was found in none of Group 1 and in all of Groups 2 and 3. After application of 0.2 ml kg^–1 test solution, T-elevation was found in 7% of Group 1 and in 93% of Groups 2 and 3. The injection of 0.4 ml kg^–1 revealed a T-elevation in 27%, 100%, and 100%, respectively, in Groups 1, 2, and 3.

This animal model demonstrated that increases in heart rate and T-elevation in the ECG during i.v. application of a common test dose (0.2 ml kg^–1) of bupivacaine are caused by epinephrine addition. Whether higher doses of bupivacaine alone can cause similar ECG changes or not requires further studies.