During induction of anaesthesia with etomidate, myoclonic muscle movements are frequent. In this study, pretreatment with a small dosage of etomidate or midazolam was compared with placebo for the prevention of myoclonic muscle movements. Sixty patients, premedicated with oral midazolam, were pretreated in a randomized double-blinded fashion with etomidate 0.05 mg/kg IV, midazolam 0.015 mg/kg IV or normal saline IV (placebo) in three groups of 20 patients each. The pretreatment was followed after 90 seconds by etomidate 0.3 mg/kg IV. One minute after onset of hypnosis, induction of anaesthesia was completed with sufentanil and rocuronium. From the time of pretreatment to completion of anaesthesia, patients were observed for myoclonic muscle movements by a single physician, blinded to group allocation. Myoclonic movements were graded on a scale of 0 to 3. The incidence of myoclonic movements was significantly lower in patients pretreated with midazolam (4 of 20) compared with placebo (18/20) (P<0.01). Midazolam 0.015 mg/kg IV, administered 90 seconds before induction of anaesthesia with etomidate, is effective in reducing etomidate-induced myoclonic muscle movements.

Sufentanil 0.3 micro g kg-1 is an effective and safe drug to reduce myoclonus after etomidate without causing any harmful side-effect.

IntroductionThe principal mechanisms of ventilator induced lung injury (VILI) have been investigated in numerous animal studies. However, prospective data on the effect of old age on VILI are limited. Under the hypothesis that susceptibility to VILI is increased in old age, we investigated the pulmonary and extrapulmonary effects of mechanical ventilation with high tidal volume (VT) in old compared to young adult animals.InterventionsOld (19.1 ± 3.0 months) and young adult (4.4 ± 1.3 months) male Wistar rats were anesthetized and mechanically ventilated (positive end-expiratory pressure 5 cmH2O, fraction of inspired oxygen 0.4, respiratory rate 40/minute) with a tidal volume (VT) of either 8, 16 or 24 ml/kg for four hours.Respiratory and hemodynamic variables, including cardiac output, and markers of systemic inflammation were recorded throughout the ventilation period. Lung histology and wet-to-dry weight ratio, injury markers in lung lavage and respiratory system pressure-volume curves were assessed post mortem. Basic pulmonary characteristics were assessed in non-ventilated animals.ResultsCompared to young adult animals, high VT (24 ml/kg body weight) caused more lung injury in old animals as indicated by decreased oxygenation (arterial oxygen tension (PaO2): 208 ± 3 vs. 131 ± 20 mmHg; P <0.05), increased lung wet-to-dry-weight ratio (5.61 ± 0.29 vs. 7.52 ± 0.27; P <0.05), lung lavage protein (206 ± 52 mg/l vs. 1,432 ± 101; P <0.05) and cytokine (IL-6: 856 ± 448 vs. 3,283 ± 943 pg/ml; P <0.05) concentration. In addition, old animals ventilated with high VT had more systemic inflammation than young animals (IL-1β: 149 ± 44 vs. 272 ± 36 pg/ml; P <0.05 - young vs. old, respectively).ConclusionsVentilation with unphysiologically large tidal volumes is associated with more lung injury in old compared to young rats. Aggravated pulmonary and systemic inflammation is a key finding in old animals developing VILI.

In this model of unilateral lung acid injury high PEEP attenuates the inflammatory cell response in the acid-injured lung, preserved oxygenation and has no deleterious effects in the opposite lung.