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Endotracheal intubation is required to keep the airway open when a patient undergoes surgery under general anaesthetic. Here we present a rare complication of endotracheal intubation.A 70-year-old woman underwent repeat pulmonary vein isolation for atrial fibrillation under general anaesthetic. Because the procedure was expected to take a long time, and because the surgeon might want to perform transoesophageal echocardiography, we chose to carry out endotracheal intubation on this patient. After the operation she showed dyspnoea, problems with swallowing and dysarthria. Physical examination showed elevation of the right pharyngeal arch and deviation of the tongue to the right. This was found to be due to hypoglossal nerve injury.Hypoglossal nerve injury is a rare complication of endotracheal intubation. There is no proven effective treatment for this complication. Prognosis is favourable: 69% of the patients recover completely in the first 6 months following intubation. Patients with this complication should receive supportive therapy, such as speech therapy and dietary modifications, to prevent aspiration.

Background Respiratory depression is a potentially fatal complication of opioid use, which may be exacerbated by simultaneous ethanol intake. In this three-way sequential crossover dose-escalating study, the influence of coadministration of oral oxycodone and intravenous ethanol was assessed on resting ventilation, apneic events and the hypercapnic ventilatory response in healthy young and older volunteers. Methods Twelve young (21 to 28 yr) and 12 elderly (66 to 77 yr) opioid-naive participants ingested one 20 mg oxycodone tablet combined with an intravenous infusion of 0, 0.5, or 1 g/l ethanol. Resting respiratory variables and the primary outcome, minute ventilation at isohypercapnia (end-tidal partial pressure of carbon dioxide of 55 mmHg or VE55), were obtained at regular intervals during treatment. Results Oxycodone reduced baseline minute ventilation by 28% (P < 0.001 vs. control). Ethanol caused a further decrease of oxycodone-induced respiratory depression by another 19% at 1 g/l ethanol plus oxycodone (P < 0.01 vs. oxycodone). Ethanol combined with oxycodone caused a significant increase in the number of apneic events measured in a 6-min window with a median (range) increase from 1 (0 to 3) at 0 g/l ethanol to 1 (0 to 11) at 1 g/l ethanol (P < 0.01). Mean (95% CI) VE55 decreased from 33.4 (27.9 to 39.0) l/min (control) to 18.6 (15.6 to 21.6) l/min (oxycodone, P < 0.01 vs. control) and to 15.7 (12.7 to 18.6) l/min (oxycodone combined with ethanol, 1 g/l; P < 0.01 vs. oxycodone). Conclusions Ethanol together with oxycodone causes greater ventilatory depression than either alone, the magnitude of which is clinically relevant. Elderly participants were more affected than younger volunteers.

Respiratory depression is a potentially fatal complication of opioid use, which may be exacerbated by simultaneous ethanol intake. In this three-way sequential crossover dose-escalating study, the influence of coadministration of oral oxycodone and intravenous ethanol was assessed on resting ventilation, apneic events and the hypercapnic ventilatory response in healthy young and older volunteers.Twelve young (21 to 28 yr) and 12 elderly (66 to 77 yr) opioid-naive participants ingested one 20 mg oxycodone tablet combined with an intravenous infusion of 0, 0.5, or 1 g/l ethanol. Resting respiratory variables and the primary outcome, minute ventilation at isohypercapnia (end-tidal partial pressure of carbon dioxide of 55 mmHg or VE55), were obtained at regular intervals during treatment.Oxycodone reduced baseline minute ventilation by 28% (P0.001 vs. control). Ethanol caused a further decrease of oxycodone-induced respiratory depression by another 19% at 1 g/l ethanol plus oxycodone (P0.01 vs. oxycodone). Ethanol combined with oxycodone caused a significant increase in the number of apneic events measured in a 6-min window with a median (range) increase from 1 (0 to 3) at 0 g/l ethanol to 1 (0 to 11) at 1 g/l ethanol (P0.01). Mean (95% CI) VE55 decreased from 33.4 (27.9 to 39.0) l/min (control) to 18.6 (15.6 to 21.6) l/min (oxycodone, P0.01 vs. control) and to 15.7 (12.7 to 18.6) l/min (oxycodone combined with ethanol, 1 g/l; P0.01 vs. oxycodone).Ethanol together with oxycodone causes greater ventilatory depression than either alone, the magnitude of which is clinically relevant. Elderly participants were more affected than younger volunteers.

Background: Rotational thromboelastometry is increasingly used to detect hyperfibrinolysis, which is a predictor of unfavorable outcome in patients with coagulation disturbances. In an in vitro study, the authors investigated which thromboelastometric hemostatic parameters could be valuable for fast diagnosis of the severity of hyperfibrinolysis and confirmed their findings in a patient population with hyperfibrinolysis. Methods: Thromboelastometry was performed after adding increasing concentrations of tissue plasminogen activator (0 to 400 ng/ml) to citrated blood samples of 15 healthy volunteers. Lysis parameters included the clotting time, maximum clot firmness, maximum lysis, and lysis onset time (LOT). The relation of tissue plasminogen activator with the LOT was further investigated in a patient population with out-of-hospital cardiac arrest and hyperfibrinolysis. Results: The LOT showed a dose-dependent association with increasing tissue plasminogen activator concentrations. Late, intermediate, or fulminant hyperfibrinolysis was associated with an average LOT (mean ± SD) of 42.7 ± 13.8, 23.2 ± 8.2, and 17.5 ± 4.6 min in the in vitro study and estimated 42.2 ± 8.3, 29.1 ± 1.2, and 14.6 ± 7.7 min in patients, respectively. The authors found a moderately negative correlation between patient plasma tissue plasminogen activator levels and the LOT (r = −0.67; P = 0.01). Conclusion: This study shows that the LOT may be used for fast detection of severe hyperfibrinolysis, with a better resolution than the maximum lysis, and should be further evaluated for optimization of therapeutic strategies in patients with severe clot breakdown.