Anesthesiology
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Over the past four decades, we have learned considerably more about the pathophysiology and treatment of drowning. This, coupled with increased emphasis in improvement in water safety and resuscitation, has produced a threefold decrease in the number of deaths, indexed to population, from drowning in the United States yearly. This review presents the current status of our knowledge of the epidemiology, the pathophysiology of drowning and its treatment, updates the definitions of drowning and the drowning process, and makes suggestions for further improvement in water safety.
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Randomized Controlled Trial
Rifampin greatly reduces the plasma concentrations of intravenous and oral oxycodone.
Oxycodone is a mu-opioid receptor agonist that is metabolized mainly in the liver by cytochrome P450 3A and 2D6 enzymes. Rifampin is a strong inducer of several drug-metabolizing enzymes. The authors studied the interaction of rifampin with oxycodone. Their hypothesis was that rifampin enhances the CYP3A-mediated metabolism of oxycodone and attenuates its pharmacologic effect. ⋯ Induction of cytochrome P450 3A by rifampin reduced the area under the oxycodone concentration-time curve of intravenous and oral oxycodone. The pharmacologic effects of oxycodone were modestly attenuated. To maintain adequate analgesia, dose adjustment of oxycodone may be necessary, when used concomitantly with rifampin.
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When switching from two-lung to one-lung ventilation (OLV), shunt fraction increases, oxygenation is impaired, and hypoxemia may occur. Hypoxemia during OLV may be predicted from measurements of lung function, distribution of perfusion between the lungs, whether the right or the left lung is ventilated, and whether the operation will be performed in the supine or in the lateral decubitus position. ⋯ Hypoxemia during OLV may be treated symptomatically by increasing inspired fraction of oxygen, by ventilating, or by using continuous positive airway pressure in the nonventilated lung. Hypoxemia during OLV may be treated causally by correcting the position of the double-lumen tube, clearing the main bronchi of the ventilated lung from secretions, and improving the ventilation strategy.
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A stimulation current of no more than 0.5 mA is regarded as safe in avoiding nerve injury and delivering adequate stimulus to provoke a motor response. However, there is no consistent level of stimulating threshold that reliably indicates intraneural placement of the needle. The authors determined the minimally required stimulation threshold to elicit a motor response outside and inside the most superficial part of the brachial plexus during high-resolution, ultrasound-guided, supraclavicular block. ⋯ Within the limitations of this study and the use of ultrasound, a stimulation current of 0.2 mA or less is reliable to detect intraneural placement of the needle. Furthermore, stimulation currents of more than 0.2 and no more than 0.5 mA could not rule out intraneural position.
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Previous experimental studies of ventilator-induced lung injury have shown that positive end-expiratory pressure (PEEP) is protective. The authors hypothesized that the application of PEEP during volume-controlled ventilation with a moderately high tidal volume (VT) in previously healthy in vivo rats does not attenuate ventilator-induced lung injury if the peak airway pressure markedly increases during the application of PEEP. ⋯ In contrast to previous reports, PEEP exacerbated lung damage and contributed to fatal outcome in an in vivo, mild overdistension model of ventilator-induced lung injury in previously healthy rats. That is, the addition of high PEEP to a constant large VT causes injury in previously healthy animals.